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Organic Psychiatry Flashcards

1
Q

Define organic psychiatric disorders.

A

Organic psychiatric disorders are directly caused by a demonstrable physical problem e.g. brain tumour

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2
Q

What is the function of the prefrontal cortex of the frontal lobe? What would the symptoms of dysfunction be?

A
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3
Q

What is the function of Broca’s area of the frontal lobe? What would the symptoms of dysfunction be?

A
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4
Q

What is the function of the motor, premotor and supplementary motor cortex of the frontal lobe? What would the symptoms of dysfunction be?

A
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5
Q

What is the function of the temporal lobe? What would the symptoms of dysfunction be?

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6
Q

What is the function of Wernicke’s area of the temporal lobe? What would the symptoms of dysfunction be?

A
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7
Q

What is the function of the parietal lobe? What would the symptoms of dysfunction be?

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8
Q

What is the function of the occipital lobe? What would the symptoms of dysfunction be?

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9
Q

What is the function of the arcuate fasciculus? What would the symptoms of dysfunction be?

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10
Q

Define delirium.

A

Delirium = acute and transient state of global brain dysfunction with clouding of consciousness due to an underlying physical problem.

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11
Q

Describe the epidemiology of delirium.

A

• Common
o 30% of medical inpatients
o 50% of post-operative patients
o 80% of elderly ITU patients

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12
Q

What are the risk factors of delirium?

A
  • Older age
  • Male
  • Pre-existing physical or mental illness (especially dementia)
  • Substance misuse
  • Polypharmacy
  • Malnutrition
  • Pain
  • Sensory impairment
  • Immobility
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13
Q

Describe the aetiology of delirium.

A

mnemonic: VITTAMIN
• Vascular, e.g. stroke, MI
• Infective: intracranial (e.g. encephalitis) and systemic (e.g. UTI/chest infection, septicaemia)
• Trauma: head injury, burns, fractures
• Toxic: Drugs and alcohol intoxication/withdrawal, poisoning, overdose.
• Autoimmune: e.g. SLE, MS
• Metabolic: liver/renal failure, electrolyte imbalance, hypoglycaemia
• Iatrogenic: deliriogenic medications e.g. sedatives, anticholinergics, opiates, steroids
• Neoplastic: SOLs

Other:
• Hypoxia: CV/respiratory disease
• Nutritional: Wernicke’s encephalopathy
• CNS: raised ICP

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14
Q

Describe the clinical presentation of someone with delirium.

A

Onset is sudden (hours-days) and symptoms fluctuate throughout the day, often worse in evening and at night.

• Altered consciousness: from drowsiness or stupor → clouded consciousness (fogginess, inability to focus) → vigilance or hyper-alertness

  • Global cognitive impairment: inattention, disorientation and poor memory.
  • Disorganised thinking and impoverished speech

• Mood changes prominent (can resemble depression or mania)
• Disorientated with poor attention and short-term memory
• Transient muddled delusions
• Illusions and hallucinations are common (most commonly visual)
• Sleep disturbances – insomnia or reversal of sleep-wake cycle common
• Behavioural changes
o Hyperactivity, agitation and aggression

  • Wandering, climbing into other patients’ beds, pulling out catheters
  • Easily identified

o Hypoactivity, lethargy, stupor, drowsiness and withdrawal

  • Quiet delirium
  • Easily missed

o Mixed - fluctuating between the 2 (commonest)

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15
Q

What are the investigations for delirium?

A
  • Physical examination + Obs (include DRE if hx of constipation)
  • MSE - ddx include depression, mania, negative symptoms of schizophrenia
  • Collateral hx
  • Check DHx (medication chart)
  • Cognitive assessment
  • Essentials:

o FBC
o U&Es

o TFTs

o Vit B12
o Glucose
o Calcium - bone profile
o MSU
o SaO2
o ECG
o CXR
o Septic screen

o HIV and syphilis serology

  • Consider

o LFTs

o Blood cultures

o CT head
o CSF
o EEG

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16
Q

How should we manage delirium?

A
  1. Treat the cause
    1. Manage aggravating factors (e.g.pain, dehydration, constipation)
    2. Stop unnecessary medications
    3. Optimise medication and emir any dentures fit
  2. Behavioural Management
    1. Frequent reorientation (e.g.clocks, calendars, verbal reminders)
    2. Good lighting(gloomy conditions increase risk of hallucinations/illusions)
    3. Address sensory problems (e.g.hearing aids, glasses)
    4. Avoid over-or under-stimulation (side room if the main ward is disruptive)
    5. Minimise change
      1. Don’t keep moving the patient
      2. One staff member to engage with the patient each shift
      3. Establish a routine (regular toileting and sleep hygiene)
    6. Remove things that can be thrown or tripped over
    7. Silence unnecessary noises (e.g.bleeping alarms)
    8. Allow safe or supervised wandering
  3. Medication
    1. Small night-time dose of benzodiazepines could promote sleep
    2. If short-term sedation is needed, low-dose typical antipsychotics (e.g.haloperidol) or benzodiazepines can be used
  4. Consider Referral
    1. Geriatrics
    2. Old-Age Psychiatry - those who suffer delirium are at increased risk of subsequent dementia
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17
Q

How can delirium be prevented?

A

o Good sleep hygiene without medication
o Minimal moves around hospital
o Encouraging mobility
o Proactive management (minimise dehydration, pain, constipation, urinary retention and sensory problems) - optimise physical health

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18
Q

What is the prognosis of delirium?

A
  • Associated with:
    • Increased mortality
    • Longer admissions
    • Higher readmissions rates
    • Subsequent nursing home placement
  • May take days to weeks to resolve
  • Some patients do not return to pre-morbid levels
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19
Q

How do we classify dementia?

A

Dementia’s can be divided into cortical and subcortical types

• Cortical e.g. Alzheimer’s

o Affects cortical functions e.g. memory, language

• Subcortical e.g. Huntington’s

o Affects functions controlled by subcortical structures e.g. thalamus and basal ganglia

o Problems include bradyphrenia (mental slowing), bradykinesia, depression, movement disorders and executive dysfunction

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20
Q

Who is affected by frontotemporal dementia (FTD)?

A
  • FTD is most commonly diagnosed in 45- to 65- year- olds.
  • Most cases are ‘sporadic’ (no known cause) but around a third are familial, showing autosomal dominance inheritance.
  • Key mutations affect three genes:
    • those coding for microtubule-associated protein tau and progranulin
    • a gene on chromosome 9
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21
Q

What are the hallmarks of FTD?

A
  • Asymmetrical anterior temporal and/or frontal lobe atrophy
    • Cortical atrophy
    • neuronal loss
    • gliosis

There’s no correlation between pathological severity and clinical symptoms

• Pick’s disease - type of FD

o Neurone’s contain Pick Bodies – rounded collections of hyperphosphorylated tau protein

• Frontotemporal lobar degenerative with tau-negative ubiquinated inclusions = FTLD-U

o Tau negative inclusions found
o Similar to those found in motor neurone disease

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22
Q

What are the clinical features and prognosis of FTD?

A

Initially, there are two main FTD subtypes:

  • Behavioural variant FTD: prominent disinhibition and personality change
  • Primary progressive aphasia: worsening speech and language problems

These often overlap, particularly later on, when memory problems emerge

Executive dysfunction, binge eating, and other compulsive behaviours can affect all sufferers.

Death usually occurs within 5-10 years

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23
Q

What is Huntington’s disease?

A

Autosomal dominant disease causes dementia and chorea

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24
Q

What is the causative mutation is HD? When is the onset?

A

Mutation of trinucleotide CAG repeat in Huntingtin gene on chromosome 4.

The longer the CAG repeat, the earlier and more severe the presentation.

Onset in early middle age

Shows anticipation: Lengthening occurs with each inheritance

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25
Q

Describe this picture

A

Coronal slices from cerebral hemispheres: healthy control (left) and HD (right). The caudate nucleus (arrows) is flattened in HD.

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26
Q

What is the pathology of HD?

A

Deposit of abnormal huntingtin protein cause atrophy of the basal ganglia, thalamus and some cortical neurone loss (mostly frontal)

CT/MRI may show caudate nucleus atrophy with lateral ventricle dilatation

EEG may be flat

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27
Q

Describe the clinical presentation of HD

A
  • Clinical changes include personality and behavioural changes: Depression, irritability and aggression.
  • Subcortical dementia emerges later
  • Chorea affects limbs, trunk, face and speech muscles and produces a wide-based lurching gait
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28
Q

What is the prognosis of HD?

A
  • No cure
  • Relative can get genetic testing
  • Death usually from intercurrent illness e.g. pneumonia but suicide is the second commonest cause of death
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29
Q

What is HIV-associated neurocognitive disorder?

A

HAND encompasses a range of neurocognitive disorders caused by HIV infection of the CNS.

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30
Q

What increases the risk of HAND?

A

The risk of developing HAND increases with

  • age
  • cardiovascular risk factors
  • hepatitis C infection
  • substance use disorder (e.g. methamphetamine)
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31
Q

Describe the clinical presentation of HAND?

A
  • Asymptomatic cognitive impairment (ACI):
    • formal testing shows mild cognitive deficits.
    • Affects 30% of people taking antiretrovirals.
  • Mild neurocognitive disorder (MND):
    • objective cognitive deficits are accompanied by noticeable problems with memory, concentration, executive function, processing speed, and sometimes motor difficulties (e.g. bradykinesia).
    • Affects 20– 30% of people takingantiretrovirals.
  • • HIV- associated dementia (HAD; also known as AIDS dementia complex (ADC) or HIV encephalopathy):
    • may occur after progression from HIV to AIDS.
    • Early apathy and withdrawal progress to subcortical dementia, with neurological symptoms, e.g. ataxia, tremor, seizures, myoclonus. MRI may show generalized atrophy and diffuse white matter changes.
    • Affects 2– 8% of people taking antiretrovirals.
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32
Q
A

NPH: CT shows dilated ventricles, disproportionate to the degree of involutional changes or cortical atrophy

33
Q

Define normal pressure hydrocephalus (NPH)?

A

Rare but potentially reversible cause of dementia affecting older adults.

Impaired CSF absorption in subarachnoid space

Normal communication between ventricles, however CSF accumulates here → hydrocephalus

No increase in CSF pressure

34
Q

What causes NPH?

A

Causes: meningitis, head injury or idiopathic (50%)

35
Q

What are the clinical features of NPH?

A

Triad of symptoms due to distortion of periventricular white matter

o Dementia (subcortical)

o Unsteady gait

o Urinary incontinence

36
Q

What is the tx of NPH?

A

A ventriculo-peritoneal shunt is first line, to allow CSF drainage into the peritoneal cavity (where the body absorbs it)

37
Q

Define Transmissible Spongiform Encephalopathies (TSEs) or Prion Disease.

A

Cell membranes contain normal prion protein (PrPc).

If this changes into a misfolded, insoluble form (PrPSc), it causes TSEs, or prion diseases.

A domino effect occurs as PrPSc turns other PrPc into PrPSc

38
Q

What Is the main TSE in humans? What causes it?

A

The main TSE in humans is

Creutzfeldt– Jakob disease (CJD);

  • the commonest type is sporadic CJD (sCJD), due to spontaneous PrPc misfolding.
  • Variant CJD (vCJD) results, rarely, from eating BSE- infected beef

CJD can also be iatrogenic (e.g. following blood transfusion) or familial.

39
Q
A
40
Q

Describe the pathophysiology of prion disease?

A

All types cause prion accumulation, leading to spongiform and amyloid changes in the cerebrum, basal ganglia, and cerebellum.

After up to 20 years’ incubation, a rapidly progressive and fatal illness is marked by dementia, motor abnormalities (e.g. ataxia), and myoclonus.

Prions are extremely resistant to disinfectants, heat, formalin, and ultraviolet and ionizing radiation, so transmission risks must be considered before exposure-prone procedures, e.g. diagnostic brain and tonsil biopsies.

Additionally, brain biopsy risks lasting damage, so is only used when there’s diagnostic uncertainty

41
Q
A
42
Q

Define amnestic disorder.

A

Profound anterograde memory loss – inability to lay down new memories from the time of brain damage onwards

43
Q

Describe the pathology of amnestic disorder. What are the causes?

A

Damage affects limbic structures dealing with explicit memory – hippocampus, mammillary bodies, parts of the thalamus and surrounding cortex

Patients may confabulate

Procedural memory is intact as cortex, basal ganglia and cerebellum are undamaged

Causes:

  • Trauma
  • Infection
  • Tumours
  • Hypoxia
  • CO poisoning
  • Korsakoff’s syndrome = most common type of amnesic syndrome
    • Due to thiamine (B1) deficiency
44
Q

How can memory be classified?

A
45
Q

What is the clinical presentation of amnestic disorders?

A
  • No new explicit memories are laid down.
  • Working memory is intact, but information is lost once it’s no longer being actively used.
  • Some people confabulate, describing things they ‘remember’ but which never happened; they’re not deliberately lying, but trying to make sense of confusing memory gaps, using any memories that come to mind.
  • There may be some retrograde amnesia (loss of memories before the damage), but other brain functions are relatively intact (unlike in delirium or dementia)
46
Q

How do we treat amnestic disorders?

A
  • Quite disabling - often needs intensive residential support
  • Prompt parenteral thiamine may prevent Wernicke encephalopathy from developing into KS (after this irreversible)
47
Q

What is Transient global amnesia? Who does it affect? What is the presentation?

A

Acute global memory loss, lasting from 1-25 hours

Patients usually over 40 and otherwise healthy

Anterograde memory affected

Patients are often bewildered – patients don’t forget their identity

48
Q

What causes transient global amnesia? What is the prognosis

A

Transient ischaemia affecting memory structures

Physical (swimming in cold water) or emotional stress

Cause unclear though ischaemic, migrainous, and epileptic mechanisms have been suggested

Neuro exam normal

Good prognosis however episodes can recur.

49
Q

What causes frontal lobe syndrome?

A

Anything which damages the frontal lobes can cause frontal lobe syndrome e.g. head injury, dementia, stroke

50
Q

What is the consequence of having FLS?

A

Executive Dysfunction

  • Poor attention and working memory
  • Poor reasoning and problem solving
  • Poor planning, decision making and judgement
  • Loss of flexibility
  • Difficulty inhibiting habitual responses.

Social Behaviour and Personality Change

  • Inappropriate behaviour (e.g. irresponsible, disinhibited, aggressive)
  • Impulsivity
  • Euphoric or fatuous mood; lability
  • Apathy, no motivation/initiative
  • Self-neglect
  • Repetitive or compulsive behaviours (e.g. compulsive eating)

Depending on part of lobes most affected, patients tend to be either apathetic (dorsolateral damage) or disinhibited and socially inappropriate (orbitofrontal damage)

Speech and motor function may be affected and frontal release signs can re-emerge.

May show utilization behaviour (inability to resist manipulating objects) e.g. grabbing and wearing someones glasses.

May also show perseveration: repeating a word or action despite losing the original stimulus.

51
Q

How do we diagnose FLS? What is the management?

A

Dx requires neuroimaging (E.g. identifying atrophy, lesions) + specialist neuropsychological testing + formal occupational therapy assessment of impairment

Unless the cause is treatable, Mx is through rehab and supportive care.

52
Q

What are the types of head injury?

A

Open: skull is penetrated causing local cerebral damage

Closed: brain damage caused by acceleration/deceleration and shearing forces

53
Q

How is traumatic brain injury (TBI) severity graded?

A

Severity is graded as mild, moderate or severe according to GCS, duration of coma and duration of post-traumatic amnesia

54
Q

What is the clinical presentation of TBI?

A

Immediate effects include concussion (brief loss of brain function), with delirium or coma in severe cases (especially closed injuries).

Once normal consciousness is regained, memory problems are common:

  • Post-traumatic amnesia: time of injury until time of recovery of memory (anterograde amnesia with disorientation and confusion). The longer it lasts the more risk of complication
  • Retrograde amnesia: memory loss of events before the injury. Doesn’t predict outcome.
55
Q

What are the psychiatric sequelae of TBI?

A

Ongoing Cognitive impairment

  • Ranges from mild deficits to severe dementia
  • Focal > global in open injury
  • Global > focal in closed head injury
  • Typically, attention, concentration, memory, processing speed, and problem- solving are affected.
  • Circumscribed and permanent anterograde amnesia can occur (amnestic syndrome)

Personality Change

  • May be subtle: exaggeration of premorbid traits or disabling (e.g. FLS)

Post-concussional syndrome (PCS)

  • 20-50% of those with mild head injury
  • Usually lasts a few weeks but 10% persist for at least a year
  • Symptoms
    • Mood: depression, anxiety, irritability
    • Cognitive: poor concentration and memory
    • Somatic: headache, dizziness, fatigue, insomnia, noise sensitivity

Depression and anxiety - affect up to 50%.

Increased risk of attempted and completed suicide. TBI can also cause ongoing psychosis.

56
Q

What is the management of TBI?

A
  • Specialist head injury services - psychological and physical rehabilitation
  • Psychotropic drugs with care
  • Education and reassurance in mild head injury
57
Q

Define Parkinson Disease. What causes it?

A

Parkinson disease (PD) is a progressive CNS disorder.

The cause is unknown (idiopathic), although genetic and environmental factors (e.g. exposure to pesticides) can increase the risk.

58
Q

What is secondary Parkinsonism?

A
59
Q

What is the pathology of PD?

A

Degeneration of dopaminergic cells in substantia nigra → depletion of dopaminergic tracts leading to the basal ganglia.

Abnormal deposits of the protein alpha-synuclein from in affected cells as Lewy bodies.

60
Q

What is the Clinical presentation of Parkinson’s disease?

A

Classic triad of extra-pyramidal symptoms

  • Tremor: pill-rolling
  • Rigidity
  • Bradykinesia

• Other signs and symptoms

o Stooped posture

o Shuffling gait
o Mask-like facies

o Swallowing difficulties

o Recurrent falls
o Constipation
o Urinary problems

61
Q

What are the psychiatric sequelae in Parkinson’s disease? How do we manage them?

A

Depression

  • Affects up to 45% of parkinson’s patients
  • Difficult to PD as depression symptoms can overlap e.g. lack of smiling and psychomotor slowing
  • Tx is same as primary depression

Parkinson’s disease dementia

  • Up to 80% of Parkinson’s patients eventually develop dementia
  • Increased mortality, carer stress and nursing home admission
  • Early symptom = bradyphrenia
  • Presence of PD before cognitive impairment = NOT lewy body dementia
  • Acetylcholinesterase inhibitors can help

Psychotic Symptoms

  • Up to 40% of patients with PD, can also be a SE of dopaminergic anti-parkinson medication
  • Visual hallucinations (often of animals or people) are common
  • Strongest predictor of nursing home placement
  • Mx: balance too much dopamine (psychosis) and too little (parkinsonism) - BALANCE
62
Q

Define Multiple Sclerosis.

A

MS is a chronic autoimmune disorder, characterized by demyelination, inflammation, and plaque formation in CNS white matter tracts.

63
Q

Describe the pathology of MS?

A

Pathology occurs at different sites at different times, causing various neurological symptoms. MS may be:

  • Relapsing– remitting (80%) initially, though symptoms later become permanent (secondary progressive form).
  • Primary progressive (10%), deteriorating without remission.
  • Benign (<10%), relapsing infrequently, and never causing permanent symptoms
64
Q

What are the psychiatric sequelae of MS?

A

May suffer embarrassing pathological affect (emotional incontinence) - excessive emotional outbursts e.g. suddenly laughing or crying for little reason.

Depression

Up to 50% of MS patients suffer from depression secondary to:

  • MS
  • Disability and pain
  • Medications e.g. steroids, baclofen, interferon

Tx: As for primary depression

Substantial increase (near 2x) in risk of suicide

Mania and psychosis also common

Half of people: Memory and concentration problems are also common

Dementia in up to 60% of people with late-stage MS

Dementia affects 60% in late stages of MS

65
Q

What are the psychiatric sequelae of strokes?

A
  • Cognitive and neurological symptoms correlate to the areas of brain damage, e.g. FLS, hemiparesis, dysphasia.
  • Other psychiatric symptoms aren’t reliably associated with specific stroke locations.
  • Depression affects up to a third of people post stroke, and impedes recovery.
    • Severity is influenced by disability, previous mental illness, and the level of social support.
    • Treatment is as for primary depression, with specialist rehabilitation.
  • Other common symptoms include anxiety, apathy, and pathological affect
66
Q

Define epilepsy.

A

Define as recurrent (2+) seizures, unproved by an immediate identifiable cause

67
Q

What is epilepsy associated with? What are possible reasons?

A
  • Increased risk of psychiatric disorder in treatment-resistant or temporal lobe epilepsy
  • High psychosocial burden and stigma of epilepsy, it neurological sequelae, underlying brain abnormalities and medication SEs
68
Q

What are the psychiatry sequelae of epilepsy? How do you manage them?

A

Depression affects up to 50% of people, and suicide rates are four times higher than in the general population.

Psychosis (6% of people) may be ‘inter-ictal’ (temporally unrelated to seizures) or ‘post- ictal’ (occurring immediately after seizures).

Other psychiatric issues include anxiety, dysthymia, cognitive impairment, and associated learning disabilities.

Mx: Antidepressants and antipsychotics are prescribed with caution, as they can reduce the seizure threshold.

69
Q

Define autoimmune encephalitis.

A

Encephalitis is inflammation of the brain parenchyma, either in response to an infectious pathogen (e.g. herpes simplex virus 1 or 2) or an autoimmune process

70
Q

What are the symptoms of encephalitis?

A

Infectious encephalitis

  • ‘flu-like symptoms, headaches, and altered consciousness level.
  • Symptoms of CNS infection such as fever, photophobia, neck stiffness, speech, motor, sensory changes and seizures

Autoimmune encephalitis

  • Insidious onset of confusion, personality or behaviour change, psychotic symptoms, sleep disturbance, and memory loss, as well as movement disorders and seizures → can be mistaken for a psychiatric presentation.

Autoimmune encephalitis is therefore a differential diagnosis for any first episode of psychosis, mania, or dementia. It’s a potentially curable cause of psychosis, so must not be missed!

71
Q

What is Anti-NMDAr encephalitis?

A

Auto-immune encephalitis caused by antibodies to the N-methyl-d-aspartate receptor, which are often generated in response to an underlying tumour (classically, an ovarian teratoma).

72
Q

What are the investigations and management of autoimmune encephalitis?

A

Investigations include neuroimaging (CT/ MRI), and blood/CSF auto-antibodies.

If present, an underlying cause for autoimmune encephalitis must be treated, alongside supportive care and immune therapies such as steroids, immunoglobulins and plasma exchange.

Residual psychiatric and memory problems can follow

73
Q

What is neurosyphilis?

A
74
Q

What are the organic and iatrogenic causes of depression?

A
75
Q

What are the organic and iatrogenic causes of mania?

A
76
Q

What are the organic and iatrogenic causes of anxiety?

A
77
Q

What are the organic and iatrogenic causes of psychosis?

A
78
Q

What are the organic and iatrogenic causes of dementia?

A

Psychiatry (13 decks)

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