ADHD is a problem with inattentiveness, over-activity, impulsivity, or a combination. For these problems to be diagnosed as ADHD, they must be out of the normal range for a child's age and development.
PubMed Health
ADHD is a problem with inattentiveness, over-activity, impulsivity, or a combination. For these problems to be diagnosed as ADHD, they must be out of the normal range for a child's age and development.
PubMed Health
Attention Deficit disorder with its etiology, types and pathophysiology clinical features, Diagnosis, Assessment, differential Diagnosis and treatment , Medical Treatment and prognosis
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It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
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5th edition of the Diagnostic and Statistical Manual of Mental Disorders
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disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. INTRODUCTION
It is a neuropsychiatric condition affecting pre-schoolers, children, adoles-
cents, and adults around the world.
Characterized by a pattern of
Diminished sustained attention
Increased impulsivity
Hyperactivity .
3. Pooled data from various studies indicate that the world wide prevalence is
5.29%.
5-10% in school going children
2-6% in adolescents
2% in adults
4. HISTORY
ADHD first was described by in 1902 George Still.
In 1920 this was termed as “minimal brain damage syndrome,”
In 1960 the condition was renamed “minimal brain dysfunction.”
ICD-9 and the DSM 2nd edition adopted the same descriptive term for the
condition— hyperkinetic syndrome of childhood.
DSM3- attention deficit /hyperactivity disorder.
In ICD-10 it is named Hyperkinetic Disorder (HKD).
5. ADHD in parents and siblings of children with ADHD is 2 to 8 times greater
than in the general population.
More prevalent in boys than in girls, ranging from 2:1 to as high as 9:1.
6. First-degree biological relatives are at high risk for developing ADHD as well
as other psychiatric disorders, including disruptive behavior disorders, anxiety
disorders, and depressive disorders.
They are also at higher risk than the general population for learning disorders
and academic difficulties.
Parents show an increased incidence of substance use disorders.
7. AETIOLOGY
Largely genetic, with a heritability of approximately 75 percent.
Genetic Factors:
The concordance rate among monozygotic twins ranges from 59 to 92 percent.
In dizygotic twins ranges from 29 to 42 percent.
First-degree relatives of children with ADHD have a 20 to 25 percent risk for
ADHD
9. Neuroanatomical Aspects:
MRI, PET, SPECT, and functional MRI studies suggested decreased volume and
activity in prefrontal areas, anterior cingulate, globus pallidus, caudate,
thalamus, hippocampus, and cerebellum in children with ADHD.
10. PET Scan
ADHD vs. Normal
White, Red, Orange = higher glucose metabolism
Blue, Green, Purple = lower glucose metabolism
NORMAL ADHD
11. Neurotransmitters –
Dopamine System- very important
Noradrenergic System
Serotonin system- weak association
ADHD patients generally cannot activate prefrontal cortex areas appropriately
in response to cognitive tasks of attention and executive functioning. Some
studies suggest that this is because dopamine (DA) and norepinephrine (NE)
dysregulation in ADHD prevents the normal “tuning” of pyramidal neurons in
the prefrontal cortex.
12. Stimulant drugs bind strongly to DAT and compete with dopamine molecules at
the DAT site to prevent reuptake of dopamine back into the presynaptic axon for
metabolism.
Tricyclic antidepressants (TCAs) and atomoxetine are potent norepinephrine
reuptake inhibitors (NRIs), perhaps restoring a more normal ratio of epinephrine
and norepinephrine.
13. Neurophysiological Factors-
Showed significantly elevated beta activity on EEG
Environmental Factors-
High lead exposure and maternal smoking have been associated with higher
rates of diagnosis of ADHD.
Higher rates of ADHD are present in children who were born prematurely
and whose mothers were observed to have maternal infection during
pregnancy.
Perinatal insult to the brain during early infancy caused by infection,
inflammation, and trauma may be contributing factors in the emergence of
ADHD symptoms.
14. DIAGNOSIS
DSM-5 Criteria
A. A persistent pattern of inattention and/or hyperactivity impulsivity that
interferes with functioning or development.
B. Several inattentive or hyperactive-impulsive symptoms were present prior to
age 12 years.
C. Several inattentive or hyperactive-impulsive symptoms are present in two or
more settings (e.g., at home, school, or work; with friends or relatives; in other
activities).
15. A-1 Inattention
At least 6 symptoms for <17 years age group.
At least 5 symptoms for 17 years or more age group.
For at least 6 months duration.
1. Often fails to give close attention to details or makes careless mistakes in
schoolwork, at work, or during other activities
2. Often has difficulty sustaining attention in tasks or play activities
3. Often does not seem to listen when spoken to directly
4. Often does not follow through on instructions and fails to finish schoolwork,
chores, or duties in the workplace
16. 5. Often has difficulty organizing tasks and activities
6. Often avoids, dislikes, or is reluctant to engage in tasks that require sustained
mental effort
7. Often loses things necessary for tasks or activities
8. Is often easily distracted by extraneous stimuli
9. Is often forgetful in daily activities.
17. A-2 Hyperactivity & Impulsivity
At least 6 symptoms for <17 years age group.
At least 5 symptoms for 17 years or more age group.
For at least 6 months duration.
1. Often fidgets with or taps hands or feet or squirms in seat
2. Often leaves seat in situations when remaining seated is expected
3. Often runs about or climbs in situations where it is inappropriate
4. Often unable to play or engage in leisure activities quietly
18. 5. Is often “on the go,” acting as if “driven by a motor”
6. Often talks excessively
7. Often blurts out an answer before a question has been completed
8. Often has difficulty waiting his or her turn
9. Often interrupts or intrudes on others.
19. D. There is clear evidence that the symptoms interfere with, or reduce the
quality of, social, academic, or occupational functioning.
E. The symptoms do not occur exclusively during the course of schizophrenia or
another psychotic disorder and are not better explained by another mental
disorder (e.g., mood disorder, anxiety disorder, dissociative disorder, personality
disorder, substance intoxication or withdrawal).
20. SUBTYPE
Combined : If both Criterion A1 (inattention) and Criterion A2 (hyperactivity-
impulsivity) are met for the past 6 months.
Predominantly inattentive : If Criterion A1 (inattention) is only met for the past 6
months.
Predominantly hyperactive/impulsive : If Criterion A2 (hyperactivity- impulsivity)
is only met for the past 6 months.
21. ICD-10 Criteria
F-90
Hyperkinetic disorder always arise in first 5 years of life
IMPAIRED INATTENTION
OVERACTIVITY
Associated Features-Disinhibition in social relations, recklessness, impulsivity,
flouting of social rules.
22. DIFFERENTIAL DIAGNOSIS
OPPOSITIONAL DEFIANT DISORDER (ODD): A pattern of negative, hostile and
defiant behavior. Symptoms include frequent loss of temper, arguing (especially
with adults), refusal to obey rules, intentionally annoying others, blaming
others.
CONDUCT DISORDER (CD): A pattern of behavior that persistently violates the
basic rights of others or society’s rules. Behavior may include aggression toward
people and animals, destruction of property, deceitfulness or theft, or serious
rule violations.
24. AUTISM ADHD
Both exhibit inattention, social dysfunction and difficult to
manage behavior.
Has no great desire to be
social.
Wants to be social. Feel sad,
confused on isolation
Repetitive patterns of behavior
are present.
Absent.
Difficulty in communication is
present.
There is no difficulty in
Communication
Children show tantrums because of
inability to tolerate a change from
there expected course of event
Due to impulsivity or poor self-
control.
28. STIMULANTS
Amphetamines and methylphenidates are two groups of stimulant medication
that have received U.S. Food and Drug Administration (FDA) approval for the
treatment of youth with ADHD.
These chemicals structurally resemble the catecholamine neurotransmitters
dopamine (DA) and norepinephrine (NE).
Improve vigilance and reaction time and reduce variability, short-term
memory, and learning of verbal and nonverbal material in children with ADHD.
Methylphenidate commonly used started 0.3-1 mg/kg tid and gradually
increased up to 60mg/day.
29. It reduce gross motor over activity, out-of-seat behavior, calling-out behavior in
the classroom, disruptiveness, impulsive behaviour.
Adverse Effects:
Common side effects include decreased appetite, weight loss, delayed onset of
sleep, headaches, stomach-aches, and increases in blood pressure and pulse.
Preschool children can experience increased irritability and crying.
30. Rebound :Rebound over activity, impulsivity, and inattention have been defined
as being more severe than reported at baseline off medication. They may occur
in the late afternoon or early evening.
long term side effect: reduce the rate of height and weight gains in developing
children with ADHD and it also increases substance use.
31. NONSTIMULANT
ATOMOXETINE HCl
Norepinephrine reuptake inhibitor
Well absorbed.
ATX has been shown to reduce ADHD behaviors in children, adolescents, and
adults.
Side effects-abdominal discomfort, decreased appetite, dizziness, vertigo
irritability and mood swings
Metabolized by the cytochrome P450 (CYP) 2D6 hepatic enzyme system.
DOSAGE-0.5-1.2mg/kg per day in children
32. TRICYCLIC ANTIDEPRESSANTS
Imipramine, Nortriptyline, Amitriptyline have been found to be effective
Lower dosages are required when compared to depression
Side effects-Fatigue and sedation, Cholestatic jaundice, tachycardia, delirium,
weight gain, constipation, skin rash, lowered seizure threshold.
CVS S/E-Slowing of cardiac conduction, thus increasing PR and QRS intervals and
thus increase the risk of cardiac arrhythmia and thus heart block
BASELINE ECG SUGGESTED BEFORE STARTING MEDICATION
33. BUPROPION
Non TCA anti-depressants
Less effective than TCA or stimulants
Starting dose for young adolescents is 75 mg twice a day to a maximum of 200
to 300 mg per day.
S/E- fatigue, dry mouth, insomnia, headache, nausea, vomiting, tremor and
skin rash.
34. ALPHA ADRENERGIC ANTAGONISTS
Clonidine and Guanfacine
Decrease impulsivity and hyperactivity
Clonidine used as alternative or adjunctive to Methylphenidate. Its sedative
effect counters insomniac effect of Methylphenidate.
S/E-Daytime Sedation
35. Clonidine needs to be discontinued very slowly to prevent rebound adrenergic
over drive-Hypertension, agitation, headache chest pain, sleep disturbance
nausea and vomiting.
So never miss the dosage.
Clonidine should not be used in presence of preexisting cardiac problem.
Guanfacine is slightly less sedating than clonidine
36. PSYCHOSOCIAL TREATMENT OF
CHILDREN
This type of treatment includes different modalities, such as :
Psychoeducation
Academic organization skill teaching and remediation
Parent training
Behavior modification
Cognitive–behavioral therapy (CBT)
Social skills training
Individual therapy.
37. Direct contingency management plus intensive behavior therapy have yielded
significant improvement.
These begin with psychoeducation about the course, risk factors, and long-
term outcomes of ADHD.
Second, the parents are encouraged to attend more carefully to their child's
behavior, particularly when the child complies.
38. Third, the parents are trained to use time out effectively.
Fourth, the parents are instructed in establishing a contingency management
or token economy system at home. Then the parents learn how to manage
noncompliant behaviors in public settings.
Finally, advances in prosocial behavior in school are supported by use of a
daily report card.
39. PROGNOSIS
Course of ADHD is variable.
Remission usually occurs between 12-20 years of age, unlikely before that.
40-60% continue to be symptomatic through adolescence, 20-40% through
adulthood.
Most cases get better as they grow. Hyperactivity usually stops by teenage.
Easy distractibility, mood swings, hot tempers & inability to complete tasks
persist.
Those continue to have symptoms are vulnerable to antisocial behavior,
substance abuse, mood disorders & learning disorders.
40. MULTIMODAL TREATMENT STUDY OF
CHILDREN WITH ADHD (MTA STUDY)
Supported by NIMH 1999
A 14-month-long randomized clinical trial involving six clinical sites comparing
four treatment strategies
More than 500 children was included
Response on medication management, behavior therapy, combination of
medication and behavior therapy and community care are compared.
All groups showed improvement over baseline; however, a combination of
medication management and behavior therapy led to greater reduction in
symptoms in children with ADHD.
41. ADULT MANIFESTATIONS OF ADHD
An approximate 2.5 % prevalence of ADHD in the population.
Utah Criteria for Adult Attention-Deficit/Hyperactivity Disorder (ADHD)
1. Retrospective childhood ADHD diagnosis
Narrow criterion: met DSM4 criteria in childhood by parent interview
Broad criterion: both 1 and 2 are met as reported by patient
a. Childhood hyperactivity
b. Childhood attention deficit
42. 2. Adult characteristics: 5 additional symptoms including ongoing difficulties
with inattention and hyperactivity and at least 3 other symptoms
Inattention
Hyperactivity
Mood Lability
Irritability and hot temper
Impaired stress intolerance
Disorganization
Impulsivity
3. Exclusions: Not diagnosed in presence of severe depression, psychosis, or
severe personality disorder
43. Adults with ADHD demonstrate higher rates of learning disorders, anxiety
disorders, mood disorders, and substance use disorder compared with the
general population.
Treatment of ADHD in adults targets pharmacotherapy, mainly long-acting
stimulants, similar to that used with children and adolescents with ADHD.