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BMS200 > wk 14, lec 1 > Flashcards

wk 14, lec 1 Flashcards

1
Q

onset of ADHD

A

< 12 years old

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2
Q

ADHD definition

A
  • Diminished sustained attention
  • Increased impulsivity or hyperactivity
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3
Q

3 presentations of ADHD

A

o Predominately inattentive presentation
o Predominantly hyperactive/impulsive presentation
o Combined presentation

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4
Q

DSM-V criteria of ADHD for kids and adolescents

A

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…

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5
Q

ADHD in kids vs adults

A
  • 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
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6
Q

DSM-V criteria in adults for ADHD

A

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

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7
Q

DSM for ADHD in kids vs adults

A

kids need 6 symptoms adults need 5

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8
Q

what brain region in ADHD causes deficits in inhibiting motor response

A

deficits in frontal cortex (executive function), dorsal striatum (caudate) and thalamus

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9
Q

deficits in attention in ADHD from which brain regions

A

putamen, PFC, and thalamus

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10
Q

challenge with temporal perception (timing) in ADHD because of

A

frontal cortex, caudate, putamen, thalamus, parietal regions and cerebellum

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11
Q

which pathway related to enhanced reward anticipation is changed in ADHD

A

– similar to substance use pathways (ventral striatum, VTA)
o More immediate reward than delayed

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12
Q

default mode netowk and alerting mode network in ADHD

A
  • Default mode network (at rest): medial PFC and posterior cingulate cortex
  • Altering mode network (attention): frontal and parietal cortex, thalamus
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13
Q

which receptors are targeted by stimulants medication in ADHD

A
  • D1 receptors and alpha-adrenoreceptors are impacted by stimulant medications
    o Stimulant medications change amount of dopamine uptake transporters
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14
Q

which side of the brain is ADHD lateralized to

A

the right, doesnt affect the left

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15
Q

time line in substance use disorder

A

chronic and relapsing

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16
Q

morbidity and mortality in substance use disorder

A

o High morbidity and mortality from overdose or infections, CVD, hepatic, neoplastic and psychiatric and social and employment

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17
Q

substance use disorder definition

A
  • Drug seeking and taking
  • Loss of control over drug intake
  • Negative affect when access to drug is withheld
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18
Q

3 stages of addiction

A
  1. acute reinforcement and drug use
  2. escalation of drug use/dependence
  3. late stage- withdrawal/incubation/relapse
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19
Q

acute reinforcement and drug use stage in addiction

A

a. Substance activates same neurological systems for motivation and drive for natural reinforcers (i.e. food)

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20
Q

stage 2 escalation of drug use/dependence in addiction

what functions undergo changes

A

a. Long term changes to brain regions and form habit
b. Executive function and inhibitory control undergo deleterious changes

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21
Q

late stage in addiction- withdrawal/incubation/relapse

what increases the relapse chances

A

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)

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22
Q

key brain areas in substance use

A
  • 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)
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23
Q

which brain area in substance use for dopamine

A

VTA

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24
Q

which brain area for GABA and acetylcholine in substance use

A

nucleus accumbens

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25
Q

which pathway is for reward

A

mesocorticolimbic pathway

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26
Q

which pathway is for emotion regulation, executive function and cognitive control

A

mesocortical pathway

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27
Q

mesocorticolimbic pathway (reward)? which NT?

A

o VTA  nucleus accumbens  reinforce and reward
 Drugs cause increase dopamine release from VTA

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28
Q
  • Mesocortical pathway (emotion regulation, executive function, cognitive control)
A

o VTA  NA  ventral pallidum  pré-frontal córtex

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29
Q

drugs affect reward system

A
  • Drugs hijack reward system
    o Less reward from usual reward- eliciting stimuli
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30
Q

which brain area is typically for habit formation and movement regulation but is altered to be a reward pathway in substance use

A

dorsal striatum

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31
Q

impaired prefrontal cortex in substance use leads to

A

loss of behavioural control and inhibition

32
Q

escalation of use and depend of drugs from

A
  • 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
33
Q

what causes a stress-evoked relapse with drugs

A

nucleus accumbens, amydgala and limbic lobes
–> CRH or cortisol trigger

34
Q

final common pathway in relapse

A

nucleus accumbens and prefrontal cortex

35
Q

limbic region and addiction

A
  • Limbic region (hippocampus and amygdala) for cue-related relapses and cravings
36
Q

Ocular adnexa

A
  • Ocular adnexa= eyelid, conjunctiva + other structures
37
Q

conjunctiva cover?

A

mucous membrane that extends over interior surface of eyelids (palpebrae) and anterior aspect of sclera (bulbar conjunctiva)

38
Q

what is outer to and inner to the palpebral (eyelids)

A

o Outer: skin
o Inner: conjunctiva

39
Q

tarsus in the palpabrae contains

A

o Tarsus (tarsal plates)- fibroelastic connective tissue

 Meibomian glands= modified sebaceous glands for tears

40
Q

cilia on lid margin (eyelashes) have what glands

A

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

41
Q

glands of zeis vs glands of moll

A

 Glands of zeis- modified sebaceous glands open into follicles at base of lashes

 Glands of moll= modified sweat glands at base of lashes

42
Q

muscles in the palpabrae and their innervation

A

o Orbicularis oculi muscle (CN VII)
o Levator palpebrae muscle (SNS)

43
Q

bulbar conjunctiva vs palpebral conjunctiva

A
  • Bublbar conjunctiva: are over the sclera, NOT cornea
  • Palpebral conjunctiva: over inner aspect of eyelid
44
Q

palpabrae conjunctiva are made of what cells and make what

A
  • 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

45
Q

tear film has 3 components

A

o Tears secreted from lacrimal glands
o Lipids secreted from sebaceous like glands
o Mucous from goblet cells

46
Q

orbital septum is found where are separates what

A
  • Fascial plane behind orbicularis oculi
  • Separates eyelid from the orbit
47
Q

orbital septum function

A

barrier to infection

48
Q

if infections get past orbital septum what happens

A
  • If infections get past orbital septum can cause orbital cellulitis
    o Leads to vision loss, intracranial infection, thrombosis
49
Q

lacrimal glands are innervated by

A

CN VII and SNS

50
Q

puncta

A

drainage route that connects to lacrimal sac then drains into inferior meatus

51
Q

types of conjunctivitis

A
  • 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
52
Q

most common bacterial conjunctivitis

A

staph auerues and s. pneumonia

53
Q

most common viral conjunctivitis

A

adenovirus

54
Q

time line of bacterial conjunctivitis? medication? vs in viral

A

self limiting

  • bacterial is more purulent discharge (pus) and shorter time frame than viral
55
Q

chlamydia and gonorrhoea in conjunctivitis can cause

A

scarring and blindness
o eradicated goblet cells and lose mucous

56
Q

viral conjunctivitis time frame

A
  • extremely infectious and self limiting
    o lasts longer than bacterial (2-4 weeks)
57
Q

hyperemia, chemises and epiphora in viral conjunctivitis

A
  • hyperemia and chemosis= red and swell
  • epiphora= excessive tearing
58
Q

infectious conjunctivitis symptoms

A
  • conjunctival injection (red eye), itchy, tearing, discharge, crusty lashes (esp in bacterial)
    o pre-auricular and submandibular lymph nodes (eps in bacterial)
59
Q

type 2 allergic inflammation causing conjunctivitis

A

rhinitis (hay fever) and asthma
o chemosis (swelling of conjunctiva)

60
Q

gonorrheal and chlamydial conjunctivitis

A
  • 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
61
Q

trachoma (opaque cornea) from what conjunctivitis

A

chlamydia

62
Q

blepharitis definition

A

inflammation of the eyelid

63
Q

causes of blepharitis

A

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)

64
Q

 sjorgren syndrome

A

autoimmune destruction of lacrimal and salivary glands

65
Q

features in blepharitis (inflamed eyelid)

A

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)

66
Q

hordeolum (stye) cause

A

staph aureus

67
Q

hordeloum (stye) symptoms? treatment?

A

o small, tender, on margin of eye
o resolve without treatment, use warm compress and hygiene

68
Q

chalazion is what type of inflammation and caused by what

A

o granulomatous inflammation
 lipid products (from bacteria breakdown or blocked sebaceous secretions) penetrate tarsal tissue

69
Q

chalazion is similar to stye but different in how? treat?

A

o inflamed, tender bump on upper eyelid
o heat and massage to treat (sometimes antibiotics)

70
Q

keratitis from

A

HSV-1 (cold sores) or HSV-2 (genital herpes)

71
Q

pathogenesis in HSV-1 (cold sores) or HSV-2 (genital herpes) causing keratitis

A

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

72
Q

what reactivates the HSV viruses to cause eye problems

A

o reactivation of HSV from stress, excessive sunlight, hormonal fluctuations in menstrual cycle

73
Q

HSV causes what eye problems

A
  • ulcers with opacities from edema  scarred and edema stroma and cornea abnormalities
  • features: pain, tearing, red eye, decreased vision, foreign-body sensation
74
Q

what is HSV-3 keratitis also known as

A

herpes zoster opthalamicus

75
Q

how does HSV3 keratitis present

A
  • Dermatitis on CN V1 dermatome (unilateral)
  • Hutchinson sign: tip of nose involved then globe is involved (75% cases)
76
Q

features in HSV-3 keratitis (AKA herpes zoster opthalamicus)

A

pain, tearing, photophobia, red eye, corneal edema, corneal hypoesthesia (decreased sensation)c

77
Q

complications in HSV-3 keratitis (AKA herpes zoster opthalamicus)

A

glaucoma, cataract, scarring, ulcer, keratitis, post-herpetic neuralgia (pain)

BMS200 (46 decks)

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