OSCE Syndrome Prep

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Last updated 2:05 AM on 6/8/26
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24 Terms

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Alzheimer’s Disease

Gradual early episodic memory loss (both encoding and retention).

On testing you may see:

(i) evidence of rapid forgetting

(ii) poor delayed recall with little benefit from cues.

Later:

(i) language

(ii) visuospatial

(iii) EF changes

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Behavioural Variant Frontotemporal Dementia (bvFTD)

Early personality and behaviour change (apathetic, disinhibition, loss of insight, empathy, motivation, or overeating). Cognition (i.e., memory) usually appears intact early.

On testing you may see:

(i) executive dysfuntion

(ii) social cognition changes

(iii) behaviour and personality difficulties

Later:

(i) behaviour changes progress to disabling

(ii) cognitive changes - rigidity, forgetfulness, planning, attention, receptive language.

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Primary Progressive Aphasia (PPA)

A gradual language decline is often presenting first.

On testing:

Logopenic PPA = slowed speech, WFD pauses. Impaired naming, repetition, word meaning preserved. AD PATHOLOGY.

Semantic variant = fluent but empty speech. Naming and understanding of word meaning severely impaired. Repetition preserved. FTD PATHOLOGY.

Nonfluent = effortful and agrammatic speech. Naming and repetition is variable. Word meaning understanding relatively preserved. FTD PATHOLOGY.

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Dementia with Lewy Bodies (DLB)

Cognitive changes FIRST in:

(i) EF

(ii) attention

(iii) visuospatial

THEN come PD motor symptoms

Often present with:

(i) visual hallucinations

(ii) hyposmia

(iii) REM sleep changes

(iiii) autonomic dysfunction

(iiiii) neuroleptic sensitivity

PD PATHOLOGY (starts in cortex first)

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Parkinson’s Disease (PDD)

MOTOR SYMPTOMS FIRST!

THEN

Cognitive changes:

(i) fluctuating attention

(ii) visuospatial

(iii) EF

(iiii) memory is spared early

PD PATHOLOGY (starts in basal ganglia → affects substantia nigra → loss of dopamine cells)

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Vascular Dementia

Often presents with a stepwise progression of decline in:

(i) slowed processing speed

(ii) EF

(iii) attention

(iiii) recall (cues can assist)

(iiiii) depression

Diagnosed via imaging

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Posterior Cortical Atrophy

Presents as a progressive:

(i) visuospatial / visuospatial decline

(ii) praxis

(iii) literacy and numeracy impair

Memory and insight are spared early

AD PATHOLOGY (Parieto-occipital regions)

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ADHD

Impaired domains since developmental periods (< 12yrs old):

(i) attention, working memory, PS, EF

AND/OR

(ii) hyperactivity/impulsivity

Needs to be across more than 1 context

Causing functional impairment

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ASD

Impaired domains since developmental periods (< 12yrs old):

(i) social communication difficulties

(ii) restrictive or repetitive behaviours/interests, sensory difficulties.

Cognition impaired:

(iii) social cognition, flexibililty, uneven profiles

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Specific Learning Disorder

Impaired domains since developmental periods (< 12yrs old):

(i) reading

(ii) written expression

(iii) maths

CANNOT BE EXPLAINED BY AN ID

NEEDS EVIDENCE OF INADEQUATE RESPONSE TO 6 MONTH INTERVENTION

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ID

Impaired domains since developmental periods (< 12yrs old):

(i) across all cognitive functions, adaptive functioning, and social functioning

(ii) memory is usually spared

SEVERITY IS GRADED BY ADAPTIVE FUNCTIONING (mild, mod, severe)

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Foetal Alcohol Spectrum Disorder (FASD)

Prenatal exposure causing pervasive impairment across cognition
(i) EF

(ii) memory

(iii) attention

(iiii) language

(iiiii) adaptive functions

(iiiiii) motor

Sentinel facial features

REQUIRES AT LEAST OR MORE THAN 3 IMPAIRED DOMAINS

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Developmental Language Disorder

Impaired domains since developmental periods (< 12yrs old):

(i) persistent receptive and/or expressive language difficulties

(ii) delayed language milestones

(iii) difficulty understanding instructs

(iiii) poor grammar, vocab, narrative skills

(iiiii) must have academic and social impacts

(iiiii) need to rule out hearing issues, ID, ASD, and environmental deprivation

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TBI (What to ask):

ASK THE FOLLOWING:

(i) what was the mechanism of injury

(ii) was there LOC?

→ yes, how long for?

(iii) was there PTA?

(iiii) what was the GCS?

(iiiii) what were their imaging findings?

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mild TBI

GCS = 13-15

LOC = less than 30 mins

PTA = less than 24 hours

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moderate TBI

GCS = 9-12

LOC = 30 minutes to 24 hours

PTA = 1-7 days

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severe TBI

GCS = 3-8

LOC = more than 24 hours

PTA = more than 7 days

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Stroke

COGNITION DEPENDS ON AREA OF STROKE

(will likely be provided in GP referral, it is unlikely we will see a patient who has JUST suffered a stroke without medical referral)

MCA: (lateral frontal/parietal/temporal)

L = aphasia

R = neglect

ACA: (medial frontal/parietal)

Leg weakness, apathy, abulia (reduced motivation/initiation)

PCA: (occipital)

visual field deficits, agnosia

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Hypoxic Brain Injury

Prominent memory impairment

→ processing speed, executive, attention, visuospatial

Severity will depend on duration of injury

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Alcohol Related Brain Injury (ARBI)

Chronic heavy alcohol use (~5-10 years)

Common cognitive impairments:

(i) EF (planning, organisation)

(ii) slowed processing speed

(iii) attention

(iiii) memory

ASK about: alcohol use history, nutrition, and memory

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Wenicke-Korsakoff Syndome

Caused by thiamine (vit B1) deficiency from chronic alcohol use.

Wernicke encephalopathy → acute

→ confusion, ataxia, eye movement abnormalities

Korsakoff syndrome → chronic

→ profound memory impairment (anterograde amnesia), EF, reduced insight, confabulation

ASK about: alcohol use history, nutrition, and memory

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Multiple Sclerosis

Can be:

Relapsing-remitting (starts here)

Secondary progressive (gradual decline)

Primary progressive (progressive worsening, no relapses/remission)

There is cognitive change in about 50% of patients

→ attention, processing speed, memory retrieval, and EF

→ fatigue and mood considerations

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Epilepsy

Cognitive changes will depend on:

→ site of seizures (i.e., TLE accompanied by verbal memory difficulties)

→ age of onset (early onset = more impaired) * cognitive reserve (more cog reserve/education/enrichment + later onset = better outcomes)

→ medication side effects (polypharmacy = reduced attention, speed, WM flow on to higher cog functions)

→ seizure burden (more seizures = more impaired)

→ mood and lifestyle factors (huge comorbidity with mental health conditions dep/anx, lots of isolation and reduced independence, reduced internal locus of control)

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Mood (Depression/Anxiety)

Attention, processing speed, recall memory (cues help), executive functions

→ complaints often exceed deficits

→ effort considerations

→ can improve with intervention