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Core clinical problems > 30. self harm > Flashcards

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
Q

management of paracetamol overdose if presenting >24 hours after ingestion

A

Check all markers and talk to toxicology

If paracetamol detected OR INR >1.3 OR ALT > 2x normal then commence acetyl-cysteine

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26
Q

referring to other teams paracetamol overdose

A

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.

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27
Q

N-acetylcysteine infusions

A

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.

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28
Q

contraindictaions to n-acetylcystine

A

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.

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29
Q

efficacy of n-acetylcystine

A

It is virtually 100% effective in preventing liver damage when given within eight hours of ingestion[7]. After eight hours, efficacy decreases sharply.

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30
Q

management of paracetamol overdose during pregnancy

A

NAC appears to be safe during pregnancy and therefore should be administered.

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31
Q

what criteria is used for liver transplant in paracetamol induced acute liver failure

A

King’s College Hospital criteria

32
Q

King’s College Hospital criteria for liver transplantation in paracetamol-induced acute liver failure

A

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
Q

features of opioid overdose

A

pinpoint pupils.
unconsciousness.
difficulties with breathing.

34
Q

management opioid overdose

A

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
Q

features seretonin syndrome

A

Neuromuscular excitation
hyperreflexia
myoclonus
rigidity
nystagmus

autonomic nervous system excitation
hyperthermia
sweating
dilated pupils

altered mental state
Confusion

36
Q

management seretonin syndrome

A

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

37
Q

pupils SS vs NMS

A

SS - dilated

NMS - normal pupils

38
Q

neuro exam SS vs NMS

A

SS - hyperreflexia, clonus

NMS - hyporeflexia, lead pipe rigidity

39
Q

when does neuroleptic malignant syndrome occur

A

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
Q

features of NMS

A

Neuro
- muscle rigidity
- hyporeflexia
- normal pupils

autonomic nervous system
- HTN
- tachycardia
- tachypnoea

mental state
- agitated delirium with confusion

41
Q

what blood test might help you differentiate SS and NMS

A

raised creatine kinase in NMS

42
Q

complications of NMS

A

Acute kidney injury (secondary to rhabdomyolysis) may develop in severe cases.

A leukocytosis may also be seen

43
Q

management of NMS

A
  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
Q

features of tricyclic overdose?

A

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
Q

ecg changes in tricyclic overdose

A

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
Q

what does the ecg in tricyclic overdose mean in terms of complications

A

Widening of QRS > 100ms is associated with an increased risk of seizures

QRS > 160ms is associated with ventricular arrhythmias

47
Q

management of tricyclic overdose

A

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
Q

presentation of alcohol withdrawal

A

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
Q

what score should you use to assess alcohol withdrawal

A

clinical institute withdrawal assessment tool (CIWA)

Patients with scores ≤8 typically do not require medication for withdrawal.

50
Q

implication of delirium tremems not being treated

A

hyperpyrexia, ketoacidosis and profound circulatory collapse

51
Q

management of delirium tremems

A

Treatment of delirium tremens/alcohol withdrawal

Chlordiazepoxide or diazepam (long acting benzos)
Lorazepam may be preferable in patients with hepatic failure

52
Q

presentation of opioid withdrawal

A

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
Q

management of opioid dependence

A

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
Q

methadone vs buprenorphine

A

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
Q

questions to screen for alcohol missuse/dependence

A

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
Q

Pharmacological management of alcohol dependence

A

disulfiram - promotes abstinence

acamprosate - reduces craving

SIGN recommends alcoholic patients should receive oral thiamine if their ‘diet may be deficient’

57
Q

disulfiram - pharmacology? patient inofrmation, contraindications

A

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
Q

acamprosate - pharamcology

A

reduces craving, known to be a weak antagonist of NMDA receptors, improves abstinence in placebo controlled trials

59
Q

harm reduction interventions opioid missuse

A

needle exchange
Offering HIV, Hep B and C screening

60
Q

complications of opioid misuse- IV drug use

A

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
Q

diagnosis of anorexia nervosa DSM-5

A
  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
Q

physiological changes anorexia nervosa

A

Most things low
BMI
Bradycardia
Hypotension
Potassium
FSH, LH
Oestrogen and testosterone

G&C raised
Growth hormone
Glucose
Salivary Glands
Cortisol
Cholesterol
Carotenemia

63
Q

management anorexia

A

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
Q

prognosis of anorexia nervosa

A

Up to 10% of patients will eventually die because of the disorder.

65
Q

complications of anorexia nervosa

A
  • 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
Q

DSM-5 bulimia nervosa

A
  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
Q

management bulimia nervosa

A

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
Q

electrolytes re-feeding

A

KPMG
The metabolic consequences include:
Hypophosphatemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance

These abnormalities can lead to organ failure.

69
Q

managing re-feeding if not eaten for > 5 days

A

If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels

70
Q

management of re-feeding

A

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
Q

risk factors for re-feeding

A

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
Q

factors which increase risk of suicide

A

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
Q

Features associated with an increased risk of completed suicide at a future date

A

efforts to avoid discovery
planning
leaving a written note
final acts such as sorting out finances
violent method

74
Q

protective features suicide

A

family support
having children at home
religious belief

75
Q

causes seretonin syndrome

A

antidepressants: SSRI, SNRI, TCA, MAOI

Drugs causing SS esp when interacting with others:
- lithium
- tramadol, pethidine
- St John’s Wort

recreational:
- ecstasy
- amphetamines

Core clinical problems (94 decks)

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