wk 14, lec 1 Flashcards
onset of ADHD
< 12 years old
ADHD definition
- Diminished sustained attention
- Increased impulsivity or hyperactivity
3 presentations of ADHD
o Predominately inattentive presentation
o Predominantly hyperactive/impulsive presentation
o Combined presentation
DSM-V criteria of ADHD for kids and adolescents
o Symptoms > 6 months and prior to age 12,
Usually need to be present in 2+ settings i.e. school and home
Interferes with social, school, or work
Predomiannetly inattentive: 6+ symptoms of inattentive and few of hypreactive
Predominantely hyperactive: 6+ symptoms of hyperactive and few of inattentive
Combined: 6+ symptoms for both
o Inattentive symptoms: poor attention, cant focus, don’t follow through on tasks, poor organization, forgetful, procrastinate…
o Hyperactive/impulsive symptoms: fidgety, cant stay seated, blurt out answers, interrupts…
ADHD in kids vs adults
- Adult presentation is different than kids
o New onset ADHD in adulthood is uncommon… does it even exist? Maybe kids masked symptoms
o High rate comorbid with mood disorder
DSM-V criteria in adults for ADHD
o Inattentive: careless mistakes, no attention, doesn’t follow instruction, poor schedule and meet deadline, procrastinate
o Hyperactive: leave seat during meetings, blurt out answers, struggle to stay quiet, talk excessively, restless
o Only need 5+ criteria, not 6 like kids
DSM for ADHD in kids vs adults
kids need 6 symptoms adults need 5
what brain region in ADHD causes deficits in inhibiting motor response
deficits in frontal cortex (executive function), dorsal striatum (caudate) and thalamus
deficits in attention in ADHD from which brain regions
putamen, PFC, and thalamus
challenge with temporal perception (timing) in ADHD because of
frontal cortex, caudate, putamen, thalamus, parietal regions and cerebellum
which pathway related to enhanced reward anticipation is changed in ADHD
– similar to substance use pathways (ventral striatum, VTA)
o More immediate reward than delayed
default mode netowk and alerting mode network in ADHD
- Default mode network (at rest): medial PFC and posterior cingulate cortex
- Altering mode network (attention): frontal and parietal cortex, thalamus
which receptors are targeted by stimulants medication in ADHD
- D1 receptors and alpha-adrenoreceptors are impacted by stimulant medications
o Stimulant medications change amount of dopamine uptake transporters
which side of the brain is ADHD lateralized to
the right, doesnt affect the left
time line in substance use disorder
chronic and relapsing
morbidity and mortality in substance use disorder
o High morbidity and mortality from overdose or infections, CVD, hepatic, neoplastic and psychiatric and social and employment
substance use disorder definition
- Drug seeking and taking
- Loss of control over drug intake
- Negative affect when access to drug is withheld
3 stages of addiction
- acute reinforcement and drug use
- escalation of drug use/dependence
- late stage- withdrawal/incubation/relapse
acute reinforcement and drug use stage in addiction
a. Substance activates same neurological systems for motivation and drive for natural reinforcers (i.e. food)
stage 2 escalation of drug use/dependence in addiction
what functions undergo changes
a. Long term changes to brain regions and form habit
b. Executive function and inhibitory control undergo deleterious changes
late stage in addiction- withdrawal/incubation/relapse
what increases the relapse chances
a. Changes to networks in reward and executive function increase likelihood of relapse in certain cues (i.e. social, environmental, stress and having small amounts of substance)
key brain areas in substance use
- Midbrain – ventral tegmental area (VTA) – dopaminergic
- Nucleus accumbens (NA) – part of the ventral striatum (basal ganglia) – GABA or acetylcholine
- Amygdala – rostral to the hippocampus
- Hippocampus
- Prefrontal cortex
- Dorsal striatum
o i.e. putamen, caudate (basal ganglia)
which brain area in substance use for dopamine
VTA
which brain area for GABA and acetylcholine in substance use
nucleus accumbens
which pathway is for reward
mesocorticolimbic pathway
which pathway is for emotion regulation, executive function and cognitive control
mesocortical pathway
mesocorticolimbic pathway (reward)? which NT?
o VTA nucleus accumbens reinforce and reward
Drugs cause increase dopamine release from VTA
- Mesocortical pathway (emotion regulation, executive function, cognitive control)
o VTA NA ventral pallidum pré-frontal córtex
drugs affect reward system
- Drugs hijack reward system
o Less reward from usual reward- eliciting stimuli
which brain area is typically for habit formation and movement regulation but is altered to be a reward pathway in substance use
dorsal striatum
impaired prefrontal cortex in substance use leads to
loss of behavioural control and inhibition
escalation of use and depend of drugs from
- Abnormal circuits are recruited and strengthened
- Dorsal striatum= habit forming areas are activated over time (shouldn’t be a reward path)
o Cue-associated drug seeking
o Goal-directed drug seeking and craving - Dorsal striatum is for regulating movements and habits usually (not reward)
- Impaired prefrontal cortex = loss of behavioural control and inhibition
what causes a stress-evoked relapse with drugs
nucleus accumbens, amydgala and limbic lobes
–> CRH or cortisol trigger
final common pathway in relapse
nucleus accumbens and prefrontal cortex
limbic region and addiction
- Limbic region (hippocampus and amygdala) for cue-related relapses and cravings
Ocular adnexa
- Ocular adnexa= eyelid, conjunctiva + other structures
conjunctiva cover?
mucous membrane that extends over interior surface of eyelids (palpebrae) and anterior aspect of sclera (bulbar conjunctiva)
what is outer to and inner to the palpebral (eyelids)
o Outer: skin
o Inner: conjunctiva
tarsus in the palpabrae contains
o Tarsus (tarsal plates)- fibroelastic connective tissue
Meibomian glands= modified sebaceous glands for tears
cilia on lid margin (eyelashes) have what glands
o Cilia on lid margin (eyelashes) with sebaceous glands and sudoriferous glands
Glands of zeis- modified sebaceous glands open into follicles at base of lashes
Glands of moll= modified sweat glands at base of lashes
Accessory lacrimal glands
glands of zeis vs glands of moll
Glands of zeis- modified sebaceous glands open into follicles at base of lashes
Glands of moll= modified sweat glands at base of lashes
muscles in the palpabrae and their innervation
o Orbicularis oculi muscle (CN VII)
o Levator palpebrae muscle (SNS)
bulbar conjunctiva vs palpebral conjunctiva
- Bublbar conjunctiva: are over the sclera, NOT cornea
- Palpebral conjunctiva: over inner aspect of eyelid
palpabrae conjunctiva are made of what cells and make what
- Palpebral conjunctiva: over inner aspect of eyelid
o Stratified columnar epithelium with goblet cells to secrete mucous and tear film
o Accessory lacrimal glands for tears
o Lymphoid follicles
tear film has 3 components
o Tears secreted from lacrimal glands
o Lipids secreted from sebaceous like glands
o Mucous from goblet cells
orbital septum is found where are separates what
- Fascial plane behind orbicularis oculi
- Separates eyelid from the orbit
orbital septum function
barrier to infection
if infections get past orbital septum what happens
- If infections get past orbital septum can cause orbital cellulitis
o Leads to vision loss, intracranial infection, thrombosis
lacrimal glands are innervated by
CN VII and SNS
puncta
drainage route that connects to lacrimal sac then drains into inferior meatus
types of conjunctivitis
- Infectious
o Bacterial (staph aureus, s. pneumonia, h. influenza, m. catarrhalis)
Chlamydia and gonococcal
o viral (adenovirus, herpes, varicella)
o parasite, fungus (uncommon) - immune mediated
o allergic, atopic, vernal
o irritants (dust, smoke), toxins/ chemicals
most common bacterial conjunctivitis
staph auerues and s. pneumonia
most common viral conjunctivitis
adenovirus
time line of bacterial conjunctivitis? medication? vs in viral
self limiting
- bacterial is more purulent discharge (pus) and shorter time frame than viral
chlamydia and gonorrhoea in conjunctivitis can cause
scarring and blindness
o eradicated goblet cells and lose mucous
viral conjunctivitis time frame
- extremely infectious and self limiting
o lasts longer than bacterial (2-4 weeks)
hyperemia, chemises and epiphora in viral conjunctivitis
- hyperemia and chemosis= red and swell
- epiphora= excessive tearing
infectious conjunctivitis symptoms
- conjunctival injection (red eye), itchy, tearing, discharge, crusty lashes (esp in bacterial)
o pre-auricular and submandibular lymph nodes (eps in bacterial)
type 2 allergic inflammation causing conjunctivitis
rhinitis (hay fever) and asthma
o chemosis (swelling of conjunctiva)
gonorrheal and chlamydial conjunctivitis
- urgent- damage conjunctiva (no tear film) and corneal damage
o cornea ulcerate and scar opacity
o gonorrhea can perforate cornea - trachoma (cornea is opaque)- chlamydia, leading cause of blindness
o inflamed conjunctiva and cornea ulcer and scar
o large follicles under superior palpebral conjunctiva
trachoma (opaque cornea) from what conjunctivitis
chlamydia
blepharitis definition
inflammation of the eyelid
causes of blepharitis
o hordeolum (stye)- purulent infection on eyelid margin
o seborrheic dermatitis or rosacea
o allergic, drug, autoimmune
sjorgren syndrome= autoimmune destruction of lacrimal and salivary glands
o infections- herpes or varicella (HSV-3)
sjorgren syndrome
autoimmune destruction of lacrimal and salivary glands
features in blepharitis (inflamed eyelid)
o red, itch, irritated, dry, gritty
often confused with conjunctivitis
o if untreated (esp in rosacea) can lead to conjunctivitis
o severe- corneal inflammation and scarring (keratitis)
hordeolum (stye) cause
staph aureus
hordeloum (stye) symptoms? treatment?
o small, tender, on margin of eye
o resolve without treatment, use warm compress and hygiene
chalazion is what type of inflammation and caused by what
o granulomatous inflammation
lipid products (from bacteria breakdown or blocked sebaceous secretions) penetrate tarsal tissue
chalazion is similar to stye but different in how? treat?
o inflamed, tender bump on upper eyelid
o heat and massage to treat (sometimes antibiotics)
keratitis from
HSV-1 (cold sores) or HSV-2 (genital herpes)
pathogenesis in HSV-1 (cold sores) or HSV-2 (genital herpes) causing keratitis
o doesn’t cause severe damage on initial infection
o then after “resolution” its lives latent in trigeminal ganglion and cause periodic reactive symptoms
can cause corneal ulceration
what reactivates the HSV viruses to cause eye problems
o reactivation of HSV from stress, excessive sunlight, hormonal fluctuations in menstrual cycle
HSV causes what eye problems
- ulcers with opacities from edema scarred and edema stroma and cornea abnormalities
- features: pain, tearing, red eye, decreased vision, foreign-body sensation
what is HSV-3 keratitis also known as
herpes zoster opthalamicus
how does HSV3 keratitis present
- Dermatitis on CN V1 dermatome (unilateral)
- Hutchinson sign: tip of nose involved then globe is involved (75% cases)
features in HSV-3 keratitis (AKA herpes zoster opthalamicus)
pain, tearing, photophobia, red eye, corneal edema, corneal hypoesthesia (decreased sensation)c
complications in HSV-3 keratitis (AKA herpes zoster opthalamicus)
glaucoma, cataract, scarring, ulcer, keratitis, post-herpetic neuralgia (pain)
