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YEAR 4 MENTAL HEALTH > Medical emergencies > Flashcards

Medical emergencies Flashcards

1
Q

What is lithium used for?

A

Mood stabilising drug used prophylactically in bipolar disorder

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2
Q

What investigations should you do before starting lithium?

A

U+Es - to check renal function as it is excreted by the kidneys
ECG - to get baseline as lithium can cause changes
T4 levels - lithium can lead to thyroid dysfunction, so check levels

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3
Q

For lithium:
1. what is theraputic range?
2. at what concentration does lithium toxicity occur
3. how is it excreted?

A
  1. 0.4-1mmol/L
  2. 1.5 mmol/L
  3. via the kidneys
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4
Q
  1. How often should lithium levels be checked?
  2. In what patients do lithium levels need to be checked more frequently?
A
  1. Li+ to be checked weekly until dose has been constant for 4 weeks.
    Then, check monthly for 6 months - if stable after this, can change to checking 3 monthly.
  2. If on diuretics, NSAIDs, ACEi (all these drugs increase lithium in blood), low salt diet or if pregnant
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5
Q

What are common side effects of lithium? (not toxicitiy, just think of side effects)

From Ox Handbook and QuesMed

A

Hypothyroidism
Nephrogenic diabetes inspidus
Fine tremor
Dry mouth
GI disturbance
Increased thirst
Increased urination
Drowsiness

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6
Q

You check lithium levels and you see that they have been rising progressively over time. What does this suggest?

A

Progressive nephrotoxicity

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7
Q

What can lithium toxicity be precipitated by?

A

Dehydration
Renal failure
Drugs - diuretics (esp thiazides), ACEi, ARBs, NSAIDs, metronidazole

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8
Q

What are features of lithium toxicity?

A
  • Coarse tremor
  • CNS disturbance: Hyperreflexia, seizure, acute confusion, dysarthria,
  • Polyuria
  • Coma
  • Arrythmias
  • Visual disturbance
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9
Q

What is the management of lithium toxicity?

A

Largely supportive and needs specialist input
main aims of management = maintain electrolyte balance, monitor renal funcion, monitor seizure control
* mild-moderate toxicity - IV fluid resuscitation with normal saline.
* alkalisation of urine. (Note: alk of urine and fluid resus help enhance excretion of drug)
* severe toxicity / if renal function is poor - haemodialysis alongside everything else
* for agitation and seizures - use benzodiazepines if needed

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10
Q

What age bracket of patient shows increased sensitivity to lithium neurotoxicity?

A

the elderly

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11
Q

Neuroleptic malignant syndrome is caused by what drugs?

A

Atypical antipsychotic
May occur with dopaminergic drugs

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12
Q

Onset of neuroleptic malignant syndrome after taking the drugs?

A

Occurs hours- days after staring antipsychotics

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13
Q

Symptoms of neuroleptic malignant syndrome?

A

Rigidity
Pyrexia
Autonomic lability e.g hypertension, tachycardia, tachypnoea
Agitated delirium with confusion

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14
Q

Investigations for Neuroleptic Malignant Syndrome?

A

Creatinine Kinase: increased in most cases
WBC: Leukocytosis
U&Es: AKI secondary to rhabdomyolysis in severe cases

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15
Q

Management of Neuroleptic Malignant Syndrome?

A

Stop the antipsychotic
Transfer patient from psych ward to medical ward
IV fluids to prevent renal failure
Dantrolene
Bromocriptine (dopa agonist) may also be used

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16
Q

What is Acute Dystonia?

A

Adverse reaction to antidopaminergic, dopamine receptor antagonist e.g. antiemetics, antipsychotics, sometimes serotonergic agents

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17
Q

Features of Acute Dystonia?

A

Involuntary contractions of face, arm, legs and larynx

Extra pyramidal side effects- onset of atypical posture or position of muscles within minutes or hours of taking med

Torticollis: twisting of neck, causes tilt at wrong angle

Oculogyric crisis: involves ocular muscles

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18
Q

Investigations for Acute Dystonia?

A

Neuromuscular testing to examine range of motion, breathing and swallowing

Vaccination history to rule out tetanus

Blood tests: rule out hypocalcaemia (bone profile), hyperventilation (ABG/VBG), hypomagnesia, Wilson’s disease

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19
Q

Treatment of Acute Dystonia?

A

Stop causative medication
Anticholinergic agents- IV
Benzodiazepines- IV
Give procyclidine for this sustained muscle contraction (this drug is an anticholinergic)

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20
Q

What is Wernicke’s encephalopathy ?

A

a neuropsychiatric disorder caused by thiamine deficiency which is most commonly seen in alcoholics

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21
Q

Who gets Wernicke’s encephalopathy ?
What are some other RARER causes ?

A

Alcoholics

Rare causes:
* persistent vomitting e.g hyperemesis G
* stomach cancer
* dietary def e.g. post bariatric surgery / starvation- such as in anorexia
* chronic dialysis

22
Q

What is the classic triad of features in Wernicke’s encephalopathy ?

A
  • Opthalmoplegia e.g. horizontal gaze palsy / nystagmus (horizontal > verticle)
  • Ataxia
  • Encephalopathy
23
Q

Pathophysiology of Wernicke’s encephalopathy ?

A

petechial haemorrhages occur in a variety of structures in the brain including the mamillary bodies and ventricle walls.

24
Q

What are features of Wernicke’s encephalopathy ?

A
  • oculomotor dysfunction
  • nystagmus (the most common ocular sign)
  • ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy
  • gait ataxia
  • encephalopathy: confusion, disorientation, indifference, and inattentiveness
  • peripheral sensory neuropathy (decreased proprioception / foot drop)

other symptoms:
* vestibular dysfunction,
* hypothermia
* hypotension
* coma

25
Q

What investigations for Wernicke’s encephalopathy ?

A

Bloods:
* decreased red cell transketolase
* MRI (increased T2 signal) involving mammillary bodies, dorsomedial thalami, tectal plate, periaqueductal area and/or around the third ventricle.

26
Q

What is treatment of Wernicke’s encephalopathy ?

A

Parenteral thiamine (IV, IM, SC)
e.g. Vitamin B substances with ascorbic acid
followed by oral thiamine

https://bnf.nice.org.uk/treatment-summaries/alcohol-dependence/#assisted-alcohol-withdrawal

27
Q

How does Wernicke’s encephalopathy relate to Korsakoff syndrome

A

Follows wernicke’s
disproportionate impairment of in memory compared to other cognitive deficits
Features:
* antegrade and retrograde amnesia
* confabulation
*

28
Q

What are adverse effecs of clozapine?

A
  • agranulocytosis (1%), neutropaenia (3%)
  • reduced seizure threshold - can induce seizures in up to 3% of patients
  • constipation
  • myocarditis: a baseline ECG should be taken before starting treatment
  • hypersalivation
29
Q

What monitoring to prevent clozapine induced agranulocytosis?

A

Montior:
FBC and leucocytes (differenical WBC count)
Weekly - up to 18 weeks
Fortnightly - up to 1 year
monthy - 1 year onwards (as part of ongoing clozapine monitoring for pt)

30
Q

How might a patient with agranulocytoiss present?

A

Think of patient presenting with fever or recurrent bacterial infections

  • fever, malaise, infection, or mouth sores
31
Q

What might examination of a patient with drug induced agranulocytosios show?

A

May show

Tacchycardia
Hypotension
Fever

32
Q

What medications can cause drug induced agranulocytosis / neutropenia

A

clozapine, antithyroid drugs (thionamides), and sulfasalazine

33
Q

How is agranulocytosis defined?

A

absolute neutrophil count <0.1 x10⁹/L or <100 neutrophils/mm³

severe agranulocytosis is emergency - urgent management

34
Q

How do you manage clozapine induced agranulocytosis

A

With all drug- induced:
stop medication suspect - neutropenia should resolve

Antibiotic prophylaxis- ( include gram-negative cover)

Escalate

35
Q

When is clozapine induced agranulocytosis most likely to occur?

A

between 6 weeks and 18 (hence why weekly FBC monitoring for first 18 weels)

36
Q

Describe the effect of chronic alcohol on the CNS?
How does this differ to effects of alcohol withdrawal on CNS?

A
  • 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)
37
Q

What is presentation of acute alcohol withdrawal?

A
  • symptoms start at 6-12 hours: tremor, sweating, tachycardia, anxiety, nausea, vomiting, diarrhoea, insomnia, muscle pain, agitation
  • peak incidence of seizures at 36 hours
38
Q

What is management for acute alcohol withdrawal?

A
  • patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised
  • first-line: long-acting benzodiazepines e.g. chlordiazepoxide or diazepam. Lorazepam may be preferable in patients with hepatic failure. Typically given as part of a reducing dose protocol
  • carbamazepine also effective in treatment of alcohol withdrawal
39
Q

Prevelance of alcohol dependence?

A

affects 4% of popN aged 16-65 in England

40
Q

How are seizures due to acute alcohol withdrawal managed?

A

First line: lorazepam 4mg IV bolus
Second line: diazepam 10mg IV bolus OR diazepam 10mg rectally
(Note:diazepam injection is contraindicated in severe liver impairment)

DO NOT use phenytoin to treat alcohol withdrawal seizures

41
Q

Prognosis of delerium tremens secondary to alcohol withdrawal?

A

15-20% mortality

42
Q

Features of delirium tremens in alcohol withdrawal?

A
  • Onset of symptoms is usually 24-72hours after alcohol cessation of reduced intake
  • Severe tremor,
  • delusions,
  • tachycardia,
  • pyrexia,
  • visual and auditory hallucinations,
  • confusion and disorientation,
  • clouding of consciousness

Passmed: peak incidence of delirium tremens is at 48-72 hours after not drinking: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

43
Q

Management of delirium tremens from alcohol withdrawal?

A
  • oral lorazepam should be used as first-line treatment.
  • If symptoms persist or oral medication is declined, parenteral lorazepam [unlicensed], or haloperidol [unlicensed] can be given as adjunctive therapy.
  • If delirium tremens develops during treatment for acute alcohol withdrawal, the withdrawal drug regimen should also be reviewed.
44
Q

When does alcohol withdrawal occur?
(and who?)

A

occurs in patients who are alcohol-dependent and who have stopped or reduced their alcohol intake within hours or days of presentation

45
Q

Investigations for Alcohol withdrawal syndrome, and why?

from bmj best practice

A
  • VBG –> may show resp alkalosis
  • FBC –> increased MCV
  • U+Es –> elec deficienceies common –> can cause cardiac arryhtmias
  • LFTs –> elevated, ggt is elevated with heavy alcohol consumption
  • blood glucose –> hypoglycaemia commonly seen with poor nutrition or heavy alcohol use
  • bone profile –> hypocalcaemia and vit d seen in alcohol dependency
  • coagulation studies –> chronic liver disease shows prolonged PT and INR
46
Q

Differentials for alcohol withdrawal?

A

Drug intoxication
Encephalitis
Meningitis
Hypoglycaemia
Wernicke’s encephalopathy
Benzodiazepine withdrawal
Thyrotoxocosis

47
Q

Complication of alcohol withdrawal?

A

Is a common cause of status epilepticus

48
Q

What is peak incidence of delirium tremens symptoms?

A

peak incidence of delirium tremens is at 48-72 hours after not drinking

49
Q

What are causes of serotonin syndrome?

A

monoamine oxidase inhibitors
SSRIs
St John’s Wort, often taken over the counter for depression, can interact with SSRIs to cause serotonin syndrome
tramadol may also interact with SSRIs
ecstasy
amphetamines

50
Q

What are features of serotonin syndrome?

A

neuromuscular excitation
* hyperreflexia
* myoclonus
* rigidity
autonomic nervous system excitation
* hyperthermia
* sweating
altered mental state
* confusion

51
Q

What is management of serotonin syndrome?

A

Management:
* supportive including IV fluids
* benzodiazepines
* more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine

52
Q

Compare and contrast neuroleptic malignant syndrome and serotonin syndrome?

YEAR 4 MENTAL HEALTH (16 decks)

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