Psych I Flashcards

(61 cards)

1
Q

What are the 3 main criteria used to define learning disability? [3]

A

Impaired intellectual function (IQ< 70)
Impaired adaptive function
Arising in developmental period (< 18 years)

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2
Q

To have a learning disability, need to have impaired adaptive function.

State and describe the 3 domains of adaptive functioning that could be impaired? [3]

A

Most will have 2+

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3
Q

State three physical associations of Fragile X syndrome [3]

A
  • Epilepsy
  • Mitral valve prolapse
  • Otitis media
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4
Q

What are the mental / behavioural disorders of Fragile X? [5]

A
  • Mental / behavioural disorder
  • Intellectual disability (mild-severe)
  • Autistic spectrum disorder (up to 50%)
  • Social anxiety, shyness, gaze avoidance
  • ADHD
  • Panic disorder
  • Stereotypic movements
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5
Q

State 5 pre-natal causes of learning disability [5]

A

Pre-natal
* Genetic syndrome
* Infections eg Rubella
* Iodine deficiency
* Pre-eclampsia
* Maternal alcohol consumption (foetal alcohol syndrome)

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6
Q

TBL

What are mild, moderate, severe and profound learning disablities (with regards to IQ classification) [4]

A

Mild 50-69
Moderate 35-49
Severe 20-34
Profound < 20

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7
Q

What is cyclothymia? [1]

A

Cyclothymia involves milder symptoms of hypomania and low mood. The symptoms are not severe enough to significantly impair their function.

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8
Q

Describe what mania/hypomania is [4]
- What’s the key difference between them? [1]

A

What is mania/hypomania?
* both terms relate to abnormally elevated mood or irritability
* with mania there is severe functional impairment or psychotic symptoms for 7 days or more
* hypomania describes decreased or increased function for 4 days or more

From an exam point of view the key differentiation is psychotic symptoms (e.g.delusions of grandeur or auditory hallucinations) which suggest mania

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9
Q

How do you differentiate bipolar disorder to borderline personality disorder? [2]

A

Differences: While both conditions involve mood swings, the duration, frequency and triggers differ significantly. In BPD, mood swings are often reactive to environmental factors and resolve quickly whereas in bipolar disorder they occur independently of environmental stimuli and persist for longer durations.

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10
Q

Describe how manage bipolar disorder in the long term [+]
- Pharmacotherapy
- Pyschological therapy
- Social support

A

Pharmacotherapy
- Lithium works to stabilise mood
- Valproate or lamotrigine
- Atypical antipsychotics like olanzapine or aripiprazole can be used adjunctively for maintenance therapy, especially in patients with frequent relapses.

Psychological Interventions:
* Cognitive Behavioural Therapy (CBT) can help individuals understand their condition better and develop coping strategies for mood swings.
* Family-focused therapy can provide education about the disorder and improve communication within the family unit.
* Interpersonal and Social Rhythm Therapy (IPSRT) aims to stabilise daily routines and sleep patterns which can help manage symptoms.

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11
Q

How do you monitor lithium treatment? [1]

What is the aim for target range of lithium levels? [1]

A

Serum lithium levels (taken 12 hours after the most recent dose) are closely monitored to ensure the dose is correct.
- The usual initial target range is 0.6–0.8 mmol/L. Lithium toxicity can occur if the dose and levels are too high.

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12
Q

TOM TIP: Sodium valproate is teratogenic.

It can cause [2] if used in pregnancy.

A

TOM TIP: Sodium valproate is teratogenic. It can cause neural tube defects and developmental delay if used in pregnancy.

There are strict rules for avoiding sodium valproate in females with childbearing potential unless there are no suitable alternatives and strict criteria are met. The Valproate Pregnancy Prevention Programme is in place to ensure this happens, which involves ensuring effective contraception and an annual risk acknowledgement form. This has been given much attention over recent years and may be tested in exams.

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13
Q

Notable potential adverse effects of lithium include? [6]

A
  • Fine tremor
  • Weight gain
  • Chronic kidney disease
  • Hypothyroidism and goitre (it inhibits the production of thyroid hormones)
  • Hyperparathyroidism and hypercalcaemia
  • Nephrogenic diabetes insipidus
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14
Q

Describe how you would manage an acute episode of bipolar disorder:
- acute manic episode [3]
- acute depressive episode [3]

A

Treatment options for an acute manic episode (as per the NICE guidelines updated 2023) include:

Antipsychotic medications (e.g., olanzapine, quetiapine, risperidone or haloperidol) are first-line
* Other options are lithium and sodium valproate
* Existing antidepressants are tapered and stopped

Treatment options for an acute depressive episode (as per the NICE guidelines updated 2023) include:
* Olanzapine plus fluoxetine
* Lamotrigine

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15
Q

A patient is exhibiting features of severe lithium toxicity, which is generally seen if serum levels are above [] mmol/l

A

patient is exhibiting features of severe lithium toxicity, which is generally seen if serum levels are above 3.5 mmol/l

NB: Generally speaking, raised lithium levels above 4 regardless of whether any symptoms are present or not, would prompt dialysis.

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16
Q

A patient has lithium toxicity, with levels above 3.5 mmol/.

How would you tx? [1]

A

This patient is exhibiting features of severe lithium toxicity, which is generally seen if serum levels are above 3.5 mmol/l. Haemodialysis is appropriate for patients experiencing severe lithium toxicity because left untreated they will develop sustained seizure activity

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17
Q

The antipsychotics most commonly used in the treatment of manic episodes or mixed episodes in bipolar affective disorder are [4]

A

The antipsychotics most commonly used in the treatment of manic episodes or mixed episodes in bipolar affective disorder are quetiapine, olanzapine, risperidone and haloperidol.

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18
Q

A 49-year-old female with a history of manic-depressive psychosis, diagnosed at 22, presents to her General Practitioner with polydipsia and polyuria. Current medication includes lithium and a steroid inhaler for bronchial asthma. Examination reveals a blood pressure (BP) of 105/70 mmHg, with a pulse of 82 bpm and regular. There are normal fasting sugar levels and no postural drop on standing.

What are the investigation findings most likely to help diagnose this condition?

Elevated serum calcium levels
Elevated serum creatinine levels
High urine osmolality and low serum osmolality
Low urine osmolality and high serum osmolality
Low urine osmolality and low serum osmolality

A

Low urine osmolality and high serum osmolality
- Lithium is the most common cause of acquired nephrogenic diabetes insipidus. Low urine osmolality and high serum osmolality are seen in diabetes insipidus (DI). It is due to a deficiency in antidiuretic hormone secretion or poor response of kidneys to ADH. DI is associated with low urine osmolality in the face of elevated plasma osmolality. There are often other signs of dehydration, including a postural drop in BP and sodium at the upper limit of the normal range. Differentiating cranial and nephrogenic DI occurs with vasopressin in the water deprivation test, with nephrogenic DI failing to respond to vasopressin.

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19
Q

Which disorded speech might you get in mania? [2]

A

pressured speech
racing thoughts

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20
Q

Describe the drug class treatment ladder for depression [5]

A

1st line SSRI.
2nd line different SSRI.
3rd line SNRI.
4th line NSSA (e.g. mirtazapine) or earlier if insomnia a big feature.
5th line mood stabiliser e.g. lithium.

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21
Q

NICE updated its depression guidelines in 2022. It now favours a simple classification of depression severity.

Describe these classifications [2]

A

‘less severe’ depression:
- encompasses what was previously termed subthreshold and mild depression
- a PHQ-9 score of < 16

‘more severe’ depression:
- encompasses what was previously termed moderate and severe depression
- a PHQ-9 score of ≥ 16

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22
Q

When switching antidepressants:
- which drugs can you perform a direct switch? [4]

A

Switching from citalopram, escitalopram, sertraline, or paroxetine to another SSRI
direct switch is possible

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23
Q

When switching antidepressants:
- which drug needs a gap of 4-7 days before starting another low dose SSRI? [1]

A

Switching from fluoxetine to another SSRI

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24
Q

When switching antidepressants:
- How do you advise switching from an SSRI to TCA? [1]
- Which exception is there to this? [1]

A

cross-tapering is recommended (the current drug dose is reduced slowly, whilst the dose of the new drug is increased slowly
- an exception is fluoxetine which should be withdrawn, the leave a gap of 4-7 days prior to TCAs being started at a low dose

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25
Switching from **citalopram, escitalopram, sertraline, or paroxetine** to **venlafaxine** - how do you do this? [1]
**direct switch is possible (caution if paroxetine used)**
26
Lecture: - What how would you classifiy someone as having mild, moderate or severe depression? [3]
**Mild** * 2 core + 2 symptoms **Moderate** * 2 core + 3 symptoms **Severe** * 2 core + 4 or more symptoms **Both core symptoms** need to present most of the time for **at least two weeks** and represent a change from normal **Also**: - can't be secondary to. substance misuse, medication or medical disorders - Need to cause signficant distress + impairment of social/occupation/ general life
27
Describe the clinical assessment you would perform for ?depression [4]
* **Psychiatric history and mental state examination** * **PHQ-9 screening tool** * **Risk assessment** (focus on suicide ideation, somatic symptoms, and psychotic symptoms) * **Focused investigations to exclude anaemia and hypothyroidism**
28
What is the prognosis of depression like? [2]
29
What are withdrawal symptoms like for antidepressants? [3]
Flu-like symptoms, dizziness and mood changes
30
You prescribe a patient an SSRI. What information would you give them about potential side effects? [5]
Risk of **GI upset**, **changes in appetite** and **weight** (loss or gain) **Confusion** and **reduced conciousness** (due to hyponatraemia) **Suicidal thoughts and behaviour** **Lower seizure threshold** **Citalopram**: prolongs QT interval In combination with other serotnergic drugs - **serotonin syndrome** (autonomic hyperactivity, altered mental state and neuromuscular excitation)
31
Which drugs should patients on SSRIs not be given with? [3] - Explain why [+]
**MOA inhibitors** and other serotonergic drugs (e.g. **tramadol**) due to risk of **SS** **Bleeding has increased risk** with **NSAIDs, aspirin, anticoagulants** Drugs that **prolong QT interval** (e.g. **antipsychotics**)
32
How long do you withdraw SSRIs for? [1] Except which drug and how long is this for? [1]
4 weeks except fluoxetine, which is 2 weeks
33
You prescribe a patient an SNRI. What information would you give them about potential side effects? [5]
**GI upset** **Dry mouth** **Neurological effects** (**headache, abnormal dreams, insomnia, confusion, convulsions**) **Suicidal thoughts and behaviour** **Hypertension**
34
Which side effect is mirtazepine particularly associated with? [1]
**Bone marrow suppression**
35
Which population should venlafaxine be avoided / used in caution with? [1]
People at risk of arrythmia - due to ischaemic heart disease
36
Which CIWA-Ar scores would indicate: - Absent or minimal withdrawal - Moderate withdrawal - Severe withdrawal
**Absent or minimal withdrawal** - **10 or less** **Moderate withdrawal** - **15 or less** **Severe withdrawal** - **Over 15**
37
Describe the basic pathophysiology alcohol withdrawal [2]
chronic alcohol consumption **enhances** **GABA** mediated **inhibition** in the **CNS** (similar to benzodiazepines) and **inhibits NMDA-type glutamate receptors** - **alcohol withdrawal** is thought to be lead to the opposite (decreased inhibitory GABA and **increased NMDA glutamate transmission**)
38
Wernicke's encephalopathy presents with which triad? [3] - What are other presenting features [+]
**Triad of:** - **opthalmoplegia** / **nystagmus** (especially **lateral rectus palsy**, **conjugate gaze palsies:** inability to move both eyes in a single horizontal & **nystagmus** - **ataxia** - **confusion** **Confusion**: - This is often one of the first noticeable symptoms. Patients may appear disoriented, unable to concentrate, or have difficulty following conversations. **Memory Deficits**: - Both anterograde and retrograde amnesia may be present, and in severe cases, this could progress to Korsakoff's syndrome. **Apathy or Agitation**: - Emotional changes including apathy, indifference, or even agitation and combativeness can occur. **Other Clinical Features** **Hypothermia**: - Although not commonly discussed, hypothermia is a known complication and can be severe in some cases. **Altered Consciousness**: - Severe deficiency can lead to coma, and potentially death, if not treated promptly. **Gastrointestinal Symptoms**: - These are not specific but can include nausea, vomiting, and abdominal pain, often preceding the neurological symptoms. Tachycardia ## Footnote **NB**: This triad of features is only seen in up to one-third of patients.
39
Describe what is meant by neuroleptic malignant syndrome [1] Describe the presentation [+]
**Rare, life threatening, idiosyncratic reaction to anti-pyschotic use** **Presentation**: - Muscular **rigidity** - **Hyperthermia** - **Altered mental state** - **Autonomic dysfunction** - **Tachycardia** - **Labile BP** - **Sweating** The majority of patients with NMS will **develop altered mental status** followed by **rigidity, fever, and finally dysautonomia.** **Altered mental status:** - often presents with **agitation and delirium**. - **Catatonia** can be present. - May progress to **severe encephalopathy and coma.** **Rigidity**: - felt as a generalised increase in tone and may be severe. Other motor abnormalities can be present. **Fever (>38º):** - less pronounced with second-generation antipsychotics. May be >40º. **Dysautonomia**: - describes abnormalities in the autonomic nervous system. Thus, often termed ‘**autonomic instability**’. - Leads to tachycardia, labile blood pressure, profuse sweating (i.e. diaphoresis) and/or arrhythmias. ## Footnote **NB**: mayb present over days!
40
Which clinical investigations would suggest NMS [3]
**Increased CK** (due to muscle rigidity), **WCC and abnormal LFTS** - If severe, **muscle necrosis and rhabdomyolysis** may develop so **AKI may occur**
41
Describe how you treat NMS [+]
**Medical emergency** - immediately transfer to acute hosptial **Immediately stop medication that caused** **Supportive therapy:** - **IV fluids** to correct rhabdomyolysis - **antihypertensive agents (e.g. clonidine)** for profound hypertension - **Paracetamol** for **fever** - **Cooling** for **hyperthermia** - **Treat electrolyte imbalance, acute kidney injury, rhabdomyolysis** - **Cardiac monitoring** is usually required due to dysautonomia - **Benzodiazepines** can help with acute behavioural disturbance and rigidity - Severe cases: **dantrolene and bromocriptine** (to reverse NMS) - Monitor for 2 weeks+ ## Footnote **NB**: - **Dantrolene**: ryanodine receptor antagonist (causes skeletal muscle relaxation). Helps treat hyperthermia and rigidity. - **Bromocriptine**: dopamine agonist. Prescribed to restore ‘dopaminergic tone’.
42
What is the triad of symptoms seen in serotonin syndrome? [3+]
**Triad of:** - autonomic, cognitive / behavioural and neurological symptoms **Autonomic**: - Blood pressure liability - Diaphoresis - Dyspnoea - Fever - Tachycardia **Cognitive**: - Changes in mental state (confusion, sometimes hypomania) agitation and insomnia **Neurological** - akathisia - hyperflexia - impaired coordination - myoclonus - tremor
43
Describe how you treat SS
**Medical emergency** Attention needs to be given to **airway, breathing and circulation** **Stop offending medications** **Cardiac monitoring** is usually required due to **dysautonomia**. **Patients** should be **monitored** and specific complications treated (e.g. **electrolyte imbalance, acute kidney injury, rhabdomyolysis**). **Benzodiazepines** if needing admission - to help with agitation, seizures, hypertonia and myoclonus Patients can be considered for **serotonin antagonists (e.g. Cyproheptadine).** - Cyproheptadine is a histamine receptor antagonist with action against serotonin receptors. **In severe cases, patients may require organ support** (e.g. intubation & ventilation, haemofiltration) and admission to intensive care.
44
**CAGE Questions** The CAGE questions can be used to screen for harmful alcohol use quickly: What are they? [4]
**C – CUT DOWN?** Do you ever think you should cut down? **A – ANNOYED?** Do you get annoyed at others commenting on your drinking? **G – GUILTY?** Do you ever feel guilty about drinking? **E – EYE OPENER?** Do you ever drink in the morning to help your hangover or nerves?
45
You have treated a person for acute alcohol withdrawal. What advice might you give with regards to the long term mangement of their alcohol dependence? [6]
Interventions in the long-term management of alcohol dependence include: **Specialist alcohol service involvement** **Alcohol detoxification programme** **Oral thiamine** to prevent Wernicke-Korsakoff syndrome **Psychological therapy** (e.g., cognitive behavioural therapy) **Acamprosate, naltrexone or disulfiram** are medications used to help maintain abstinence **Informing the DVLA** (their driving licence will be revoked until an extended period of abstinence)
46
How do you treat delirium tremens? [4]
**Sedation** (diazepam or lorazepam) **Fluids** **Electrolyte replacements** **High potency vitamins**
47
Describe the pathophysiology of WE [2]
**Thiamine** is an essential **cofactor** for several metabolic reactions in the body. - **storage** occurs for a **maximum of 18 days** meaning a moderate consumption of thiamine is needed to maintain stores. **Thiamine deficiency** leads to **neuronal injury** - In chronic disease, there is evidence of **neuronal loss**, most notably in the **medial thalamus**
48
How would you differentiate DT with WE? [2]
**DT** is associated with **hyperthermia** rather than **hypothermia** in **WE**. - DT iss usually associated with a history of having significantly reduced alcohol intake in the prior 5 days.
49
How do you tx WE? [2]
WE is managed through urgent **administration of parenteral (not oral) thiamine for a minimum of 5 days.** - **Oral treatment** should follow **parenteral treatment.** **Care** must be taken when **administering glucose** to those suspected of exhibiting WE as **glucose metabolism requires thiamine and such metabolisis will further reduce thiamine levels**. - **Thiamine** must be administered **before** or **concurrently** with any **glucose administration.**
50
Describe the features of KS [4]
**Korsakoff syndrome** - KS is characterised by **profound memory defects**. Interestingly, **long-term memory is relatively preserved** in the condition. **Memory deficit**: - anterograde and retrograde **Confabulation**: - stories made up to fill gaps in memory **Poor insight**: - unaware of their illness **Global cognitive dysfunction:** - seen in some patients. Significant impairment in mental function with the development of dementia
51
**Cane criteria** is the diagnostic criteria proposed for WE. Based on the presence of ≥2 of the following criteria in patients with chronic alcoholism [4]
* Dietary deficiency * Oculomotor abnormalities * Cerebellar dysfunction * Altered mental status or mild memory impairment
52
Describe the typical natural history of NMS [1]
**NMS will typically occur within the first two weeks of starting an antipsychotic.** However, it can occur after a single dose or after many years of using the medication.
53
What impact may NMS have on Na levels? [1] Why? [1]
**Hyponatremia** may occur secondary to **inappropriate secretion of antidiuretic hormone or dehydration.**
54
Withdrawal symptoms occur at different times after alcohol consumption ceases> What are these with for: 6-12 hours: [4] 12-24 hours: [1] 24-48 hours: [1] 24-72 hours: [1]
**6-12 hours**: tremor, sweating, headache, craving and anxiety **12-24 hours:** **h**allucinations **24-48 hours:** **s**eizures **24-72 hours:** **d**elirium tremens ## Footnote **HSD** !
55
Describe the aetiology and pathophysiology of serotonin syndrome [+]
**Overstimulation** of **serotonergic receptors** - **SSRIs** are the most **commonly implicated medications** (e.g. **citalopram, fluoxetine**) - Also due to **increased release of serotonin**: **amphetamines, MDMA (ecstasy), cocaine** - **Impaired serotonin reuptake**: **SSRIs, SNRIs, MDMA, tricycle antidepressants** - **Inhibit serotonin metabolism:** **Monoamine oxidase inhibitors** - **Serotonin receptor agonists:** **Buspirone**, **Triptans**
56
NOTE: SS secondary to the use of **[drug class]** is usually more severe and can be fatal.
NOTE: SS secondary to the use of **monoamine oxidase inhibitors** is usually more severe and can be fatal.
57
**Hunter criteria** - SS can be diagnosed in a patient taking a serotonergic agent (e.g. SSRI) and presents with one of the following features [5]
**SSRI** + * **Spontaneous clonus** * **Inducible/ocular clonus and agitation or diaphoresis** * **Tremor and hyperreflexia** * **Hyperthermia, hypertonia, and ocular/inducible clonus**
58
**dantrolene** - dantrolene may be useful in selected cases - thought to work by decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum
59
**B1**
60
Describe the DSM-V diagnostic criteria for acute stress disorder [+]
The diagnosis of an acute stress disorder is **initially dependent on exposure to trauma.** The presence of **nine or more of the following 14 symptoms** from the below 5 categories is consistent with the diagnosis of acute stress disorder: * **Intrusion symptoms** * **Negative mood** * **Dissociative symptoms** * **Avoidance symptoms** * **Arousal symptoms**
61
# PM What is the first and second line mx for acute stress disorder? [2]
**trauma**-**focused** **cognitive**-**behavioural therapy** (**CBT**) is usually used first-line **benzodiazepines** * sometimes used for acute symptoms e.g. agitation, sleep disturbance * should only be used with caution due to addictive potential and concerns that they may be detrimental to adaptation