30. self harm Flashcards

1
Q

History suicide attempt

A

mental health
- event exploring: intention - end life or harm, triggers, impulsive or planned, note leaving, anything that made you hesitate?
- future risk exploring: how do you feel about it now? regret?
- next steps exploring: support, services, sectioning

physical health
- injury: timing, object used - rusty, tetanus? etc
- overdose : timing, strength and amount of drug, staggered? mixed overdose? what drugs are they normally on? OTC? alcohol involved?
- symptoms since: vomiting, black stool, abdo pain, colour of skin change, confusion, sob

MHx:
DHx: smoking, alcohol, recreational drugs? allergies, look out for any drugs that could be taken in overdose?
FHx:

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2
Q

principles of different ways to manage overdose

A

Prevention of absorption
Activated charcoal

Active elimination
Haemodialysis for ethylene glycol, lithium, methanol, phenobarbital, salicylates, and sodium valproate;
Alkalinisation of the urine for salicylates.

Removal from the GI tract
Gastric lavage is rarely required; for substances that cannot be removed effectively by other means (e.g. iron), it should be considered only if a life-threatening amount has been ingested within the previous hour.

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3
Q

ABCDE assessment overdose

A

ABCDE
A
Are they managing their airway?
B
Maintain airway, if RR low may need to bag-valve-mask
C
VBG, ABG if abnormal O2/RR
ECG !!!!
Maintain blood pressure with fluids
D
E
Temperature: hypothermia and hyperthermia

Examination
GI exam
Liver flap

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4
Q

alcohol poisoning features

A

ataxia, nystagmus, dysarthria, drowsiness

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5
Q

what are the risks associated with alcohol poisoning? management?

A

Risks: aspiration, hypotension, acidosis, coma, hypoglycaemia

Management:
Maintain clear airway
Monitor blood glucose and manage hypoglycemia if it occurs

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6
Q

aspirin poisoning features

A

hyperventilation (resp compensation for acidosis), tinnitus, deafness, vasodilation and sweating

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7
Q

risks and management aspirin poisoning

A

Risks: metabolic acidosis

Use plasma-salicylate concentration to guide management

Management:
Activated charcoal
Replace fluids and correct hypokalemia (important to correct before sodium bicarbonate)
IV sodium bicarbonate (urinary alkalinisation)
Haemolysis

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8
Q

features paracetamol poisoning

A

First 24 hours: few or non-specific symptoms eg feeling tired, abdominal pain, or nausea

Next few days: absence of symptoms

4+ days: yellowish skin, blood clotting problems, and confusion occurs as a result of liver failure. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis.

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9
Q

estimating risk of severe liver damage from amount of paracetamol ingested

A

Less than 150 mg/kg - unlikely.
More than 250 mg/kg - likely.
More than 12 g total - potentially fatal.

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10
Q

examination paracetamol overdose

A

GI exam

If ALF develops, the following may be seen: jaundice, hepatic flap, encephalopathy and tender hepatomegaly.

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11
Q

define acute liver failure

A

elevated LFTs
coagulopathy (INR>1.5)
encephalopathy.

Without pre-existing cirrhosis. Illness course <26 weeks (except wilsons, reactivation of hep b, autoimmune hepatitis)

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12
Q

what criteria do you use to grade hepatic encephalopathy

A

west haven criteria

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13
Q

west haven criteria for heptic encephalopathy

A

grades:

  1. Behaviour changes, altered sleep-wake cycle
  2. Asterixis, lethargy, disorientation
  3. More severe, somnolence COedema 25-35%
  4. Coma, COedema 65-75%
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14
Q

risk to brain liver failure

A

When the liver fails, ammonia levels increase→ astrocyte swelling → cerebral oedema → Intracranial Hypertension → herniation

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15
Q

cerebral oedema in liver fialure, assessment and manageemnt

A

west haven criteria

Ammonia levels correlate with risk of ICH
<75 → rare
>100 → high grade hepatic encephalopathy
>200 → ICH

CT head
Elevate bed to 30 degrees
Net even fluid balance w CRRT
Allow for hyperventilation
Induce hypernatremia to 145-155 w NaCl 3% to reduce water into brain
Mannitol

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16
Q

liver fialure and glucose

A

The liver stores glycogen and is the site of gluconeogenesis

When the liver fails, this leads to hypoglycemia

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17
Q

liver failure and coagulation

A

The liver synthesises clotting factors and anticoagulants
When the liver fails, increased risk of bleeding and of clotting

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18
Q

liver failure and immunity

A

The liver decreases risk of infection and kupffer cell → innate immunity
Have a low threshold for empirical abx

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19
Q

how does paracetamol overdose and liver fialure lead to metabolic acidosis

A

NAPQI inhibits aerobic metabolism → anaerobic metabolism → lactic acidosis

Acute liver failure → failure to metabolise lactate → lactic acidosis

Shock → hypoperfusion → lactic acidosis

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20
Q

investigations paracetamol overdose

A
  • U&E
  • LFT
  • clotting
  • ABG for acisosis
  • monitor glucose hourly (capillary glucose measurement)
  • paracetamol level
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21
Q

when should you take paracetamol level

A

Paracetamol level: take paracetamol level four hours post-ingestion, or as soon as the patient arrives if:

Time of overdose is greater than four hours.

Staggered overdose (in staggered overdoses, the level is not interpretable except to confirm ingestion).

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22
Q

Management paracetamol overdose if presenting within 1 hour of ingestion

A
  1. Activated charcoal
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23
Q

Management paracetamol overdose if presenting after 1 hour of ingetsing paracetamol

A
  1. Check level of paracetamol in the blood at or after 4 hours
    + Commence acetyl cysteine if above treatment line or if it is more than 8 hours after they ingested > 150 mg/kg
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24
Q

management of paracetamol overdose - staggered overdose

A

Commence acetyl-cysteine

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25
management of paracetamol overdose if presenting >24 hours after ingestion
Check all markers and talk to toxicology If paracetamol detected OR INR >1.3 OR ALT > 2x normal then commence acetyl-cysteine
26
referring to other teams paracetamol overdose
Refer to ICU if there is fulminant liver failure - those treated with N-acetylcysteine (NAC) to the medical team and all para-suicides to the psychiatric team.
27
N-acetylcysteine infusions
First infusion: initial loading dose of 150 mg/kg body weight over 1 hour. Second infusion: 50 mg/kg over the next 4 hours. Third infusion: 100 mg/kg over the next 16 hours. The patient should receive a total dose of 300 mg/kg body weight over a 21-hour period. A ceiling weight of 110 kg should be used when calculating the dose for obese patients.
28
contraindictaions to n-acetylcystine
There are now no specific contra-indications to acetylcysteine use. Even if there is a previously reported reaction, the benefits of treatment outweigh the risks.
29
efficacy of n-acetylcystine
It is virtually 100% effective in preventing liver damage when given within eight hours of ingestion[7]. After eight hours, efficacy decreases sharply.
30
management of paracetamol overdose during pregnancy
NAC appears to be safe during pregnancy and therefore should be administered.
31
what criteria is used for liver transplant in paracetamol induced acute liver failure
King's College Hospital criteria
32
King's College Hospital criteria for liver transplantation in paracetamol-induced acute liver failure
Arterial pH <7.3 or arterial lactate >3.0 mmol/L after adequate fluid resuscitation; OR If all three of the following occur in a 24-hour period: Creatinine >300 μmol/L. PT >100 seconds (INR >6.5). Grade III/IV encephalopathy. Strongly consider transplantation if: Arterial lactate >3.5 mmol/L after early fluid resuscitation.
33
features of opioid overdose
pinpoint pupils. unconsciousness. difficulties with breathing.
34
management opioid overdose
IV or IM naloxone : Rapid onset and short half life so need more than one dose often 1. Initially 400 micrograms then 800 micrograms for up to 2 doses at 1-minute intervals 2. if no response to preceding dose, then increased to 2 mg for 1 dose 3. if still no response (4 mg dose may be required in seriously poisoned patients)
35
features seretonin syndrome
Neuromuscular excitation hyperreflexia myoclonus rigidity nystagmus autonomic nervous system excitation hyperthermia sweating dilated pupils altered mental state Confusion
36
management seretonin syndrome
supportive including IV fluids benzodiazepines more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine
37
pupils SS vs NMS
SS - dilated NMS - normal pupils
38
neuro exam SS vs NMS
SS - hyperreflexia, clonus NMS - hyporeflexia, lead pipe rigidity
39
when does neuroleptic malignant syndrome occur
drug reaction to starting antipsychotics It may also occur with dopaminergic drugs (such as levodopa) for Parkinson's disease, usually when the drug is suddenly stopped or the dose reduced.
40
features of NMS
Neuro - muscle rigidity - hyporeflexia - normal pupils autonomic nervous system - HTN - tachycardia - tachypnoea mental state - agitated delirium with confusion
41
what blood test might help you differentiate SS and NMS
raised creatine kinase in NMS
42
complications of NMS
Acute kidney injury (secondary to rhabdomyolysis) may develop in severe cases. A leukocytosis may also be seen
43
management of NMS
1. stop antipsychotic 2. transfer to medical ward - may be ICU + IV fluids to prevent renal failure + dantrolene may be useful in selected cases + bromocriptine, dopamine agonist, may also be used
44
features of tricyclic overdose?
Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision. Features of severe poisoning include: arrhythmias seizures metabolic acidosis coma
45
ecg changes in tricyclic overdose
ECG changes include: sinus tachycardia widening of QRS prolongation of QT interval Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias
46
what does the ecg in tricyclic overdose mean in terms of complications
Widening of QRS > 100ms is associated with an increased risk of seizures QRS > 160ms is associated with ventricular arrhythmias
47
management of tricyclic overdose
IV bicarbonate - first-line therapy for hypotension or arrhythmias - indications include widening of the QRS interval >100 msec or a ventricular arrhythmia + other drugs for arrhythmias
48
presentation of alcohol withdrawal
6-12 hours : minor alcohol withdrawal symptoms: tremor, anxiety, headache. subside by 40-50 hours 12-24 hours alcoholic hallucinosis (auditory and visual, frightening, may last 5-6 days) 12-48 hours seizures 48-72 hours delirium tremens : coarse tremor, agitation, fever, tachycardia, profound confusion, delusions, hallucinations
49
what score should you use to assess alcohol withdrawal
clinical institute withdrawal assessment tool (CIWA) Patients with scores ≤8 typically do not require medication for withdrawal.
50
implication of delirium tremems not being treated
hyperpyrexia, ketoacidosis and profound circulatory collapse
51
management of delirium tremems
Treatment of delirium tremens/alcohol withdrawal Chlordiazepoxide or diazepam (long acting benzos) Lorazepam may be preferable in patients with hepatic failure
52
presentation of opioid withdrawal
flu-like manner (runny nose, eyes) GI upset (abdo pain, diarrhoea) Sympathetic hyperactivity (tachycardia and hypertension, dialted pupils, sweating, goose bump skin) central nervous system (CNS) stimulation
53
management of opioid dependence
specialist drug dependence clinics maintenance therapy or detoxification 1. methadone or buprenorphine as first line for opioid detox Compliance monitored urine urinalysis detox should normally last up to 4 weeks in an inpatient/residential setting and up to 12 weeks in community
54
methadone vs buprenorphine
methadone is a full agonist of the mu-opioid receptor - binds to these receptors in the brain and fully activates them. This action can relieve withdrawal symptoms and cravings. Has a long half-life buprenorphine is a partial agonist of the mu-opioid receptor. It binds to the mu-opioid receptors in the brain but only partially activates them. This partial activation is enough to alleviate cravings and withdrawal symptoms in individuals with opioid dependence. Furthermore, the binding of buprenorphine to the mu-opioid receptor is very strong, or 'high affinity,' meaning it can displace other opioids from these receptors and prevent them from exerting their effects. SAFER PROBLEM IF YOU USE ALONGSIDE
55
questions to screen for alcohol missuse/dependence
For alcohol use CAGE (Cutting down, Annoyance by criticism, Guilty feeling, and Eye-openers). Ask “Have you ever: (1) felt the need to cut down your drinking; (2) felt annoyed by criticism of your drinking; (3) had guilty feelings about drinking; and (4) taken a morning eye opener?”
56
Pharmacological management of alcohol dependence
disulfiram - promotes abstinence acamprosate - reduces craving SIGN recommends alcoholic patients should receive oral thiamine if their 'diet may be deficient'
57
disulfiram - pharmacology? patient inofrmation, contraindications
promotes abstinence - alcohol intake causes severe reaction due to inhibition of acetaldehyde dehydrogenase. Patients should be aware that even small amounts of alcohol (e.g. In perfumes, foods, mouthwashes) can produce severe symptoms. Contraindications include ischaemic heart disease and psychosis
58
acamprosate - pharamcology
reduces craving, known to be a weak antagonist of NMDA receptors, improves abstinence in placebo controlled trials
59
harm reduction interventions opioid missuse
needle exchange Offering HIV, Hep B and C screening
60
complications of opioid misuse- IV drug use
Overdose - respiratory depression Infection - viral infection secondary to sharing needles : HIV, hep B&C - Bacterial infection secondary to injection : infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis - cellulitis - abscesses - ulcers Blood clots - Venous thromboembolism Psychosocial impact - craving, interfere with daily life, financial --> crime, prostitution, homelessness
61
diagnosis of anorexia nervosa DSM-5
1. restriction of energy intake --> impact 2. intense fear of gaining weight 3. disturbance in the way in which one's body weight or shape is experienced
62
physiological changes anorexia nervosa
Most things low BMI Bradycardia Hypotension Potassium FSH, LH Oestrogen and testosterone G&C raised Growth hormone Glucose Salivary Glands Cortisol Cholesterol Carotenemia
63
management anorexia
adults one of: - individual eating-disorder-focused cognitive behavioural therapy (CBT-ED) - Maudsley Anorexia Nervosa Treatment for Adults (MANTRA) - specialist supportive clinical management (SSCM). children 1. 'anorexia focused family therapy' 2. CBT
64
prognosis of anorexia nervosa
Up to 10% of patients will eventually die because of the disorder.
65
complications of anorexia nervosa
- refeeding syndrome -> cardiac failure - peripheral oedema secondary to RFS - anaemia - electrolyte : hypophosphatemia, hypomagnesemia - acute thiamine deficiency - hypothyroid - more at risk of liver failure following paracetamol overdose
66
DSM-5 bulimia nervosa
1. recurrent episoses of binge eating with a sense of lack of control during 2. recurrent inappropriate compensatory behaviour in order to prevent weight gain 3. the binge eating and compensatory behaviours both occur, on average, at least once a week for three months.
67
management bulimia nervosa
ref for specialist care adults 1. bulimia-nervosa-focused guided self-help 2. eating-disorder-focused cognitive behavioural therapy (CBT-ED) children 1. children should be offered bulimia-nervosa-focused family therapy (FT-BN)
68
electrolytes re-feeding
KPMG The metabolic consequences include: Hypophosphatemia Hypokalaemia Hypomagnesaemia Abnormal fluid balance These abnormalities can lead to organ failure.
69
managing re-feeding if not eaten for > 5 days
If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels
70
management of re-feeding
Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and supplements Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)
71
risk factors for re-feeding
BMI < 16 kg/m2 Unintentional weight loss >15% over 3-6 months Little nutritional intake > 10 days Hypokalaemia, Hypophosphatemia or hypomagnesaemia prior to feeding (unless high)
72
factors which increase risk of suicide
male sex (hazard ratio (HR) approximately 2.0) history of deliberate self-harm (HR 1.7) alcohol or drug misuse (HR 1.6) history of mental illness depression schizophrenia: NICE estimates that 10% of people with schizophrenia will complete suicide history of chronic disease advancing age unemployment or social isolation/living alone being unmarried, divorced or widowed
73
Features associated with an increased risk of completed suicide at a future date
efforts to avoid discovery planning leaving a written note final acts such as sorting out finances violent method
74
protective features suicide
family support having children at home religious belief
75
causes seretonin syndrome
antidepressants: SSRI, SNRI, TCA, MAOI Drugs causing SS esp when interacting with others: - lithium - tramadol, pethidine - St John's Wort recreational: - ecstasy - amphetamines