CCT / CBL Mix Flashcards

1
Q

Definition of hyperkalaemia:

A

Serum potassium concentration >5.3mmol/L.

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2
Q

How to classify different causes of hyperkalaemia?

A

Causes of hyperkalaemia may be broken down into causes of impaired excretion of potassium from the kidney, increased release of potassium from cells, and “pseudohyperkalaemia” / artefact.

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3
Q

Skim the list of hyperkalaemia due to impaired excretion:

A
  • Acute kidney injury
  • Chronic kidney disease
  • ACE inhibitors or angiotensin receptor blockers
  • Potassium-sparing diuretics (e.g. spironolactone)
  • NSAIDs
  • Heparin/low molecular weight heparin (which inhibits aldosterone release)
  • Ciclosporin
  • High dose trimethoprim
  • Hypoaldosteronism (e.g. renal tubular acidosis type 4)
  • Addison’s disease
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4
Q

Skim the list of hyperkalaemia due to increased release from cells:

A
  • Lactic acidosis
  • Insulin deficiency
  • Rhabdomyolysis
  • Tumour lysis syndrome
  • Massive haemolysis
  • Digoxin toxicity (NB: This can be precipitated by hypokalaemia)
  • Beta-blockers.
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5
Q

Artefact causes of hyperkalaemia:

Important to think about when in a primary care setting.

A
  • Haemolysis (traumatic venepuncture, prolonged tourniquet use, fist clenching)
  • Delayed analysis (K+ leaks out of red blood cells)

Suspect this when:
- A mild rise in potassium with all other U&E results normal
- Consider spurious results in absence of:
- Acute illness (e.g. AKI, acidosis)
- Co-morbidities (elderly, renal, endocrine, CCF)
- Causative medications

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6
Q

Talk through the ECG changes seen in hyperkalaemia in order of severity.

A
  1. 5mmol = Tall tented T-waves.
  2. 6mmol = P waves flatten / Prolonged PR.
  3. 7mmol = Wide QRS
  4. 8mmol = Sine wave pattern
  5. 8mmol = Can cause Vfib
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7
Q

What is ‘severe’ hyperkalaemia?

A

> 6.5mmol K+

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8
Q

How to treat severe hyperkalaemia?

A

Treat K+ >6.5mmol/L or any ECG changes with the following;

  1. Give 10ml of 10% calcium gluconate (or chloride) over 10 mins - this is cardioprotective.
  2. Intravenous insulin (10U soluble insulin) in 25g GLUCOSE (50mL of 50% or 125ml of 20% glucose) - insulin causes intracellular K+ shift and glucose to required to prevent hypoglycaemia.
  3. Nebulised salbutamol - also causes intracellular K+ shift.
  4. Calcium resonium increases K+ excretion into urine (MH)

Loop diuretics can also be used (but longer to act).
Dialysis if not responding to treatment.

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9
Q

SIADH causes what?

A

Euvolemic hyponatraemia

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10
Q

How is SIADH managed?

A

Management revolves around offloading this excess water:

  1. Fluid restriction (up to 750ml/day) and treat underlying cause.
  2. ADH antagonists (e.g. tolvaptan, deomeclocycline).
  3. Oral sodium and furosemide.
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11
Q

How does the urine change in patients with SIADH?

A

The urine becomes more concentrated as less water is excreted by the kidneys.

Therefore patients with SIADH have a “high urine osmolality” and “high urine sodium”.

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12
Q

Symptoms of SIADH:

A
  • Headache
  • Fatigue
  • Muscle aches and cramps
  • Confusion
  • Severe hyponatraemiacan cause seizures and reduced consciousness
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13
Q

There is no reliable test for SIADH, therefore it is a diagnosis of exclusion.

  • what other investigations should be done?
A
  • Negativeshort synacthen testto excludeadrenal insufficiency
  • No history of diuretic use
  • No diarrhoea, vomiting, burns, fistula or excessive sweating
  • No excessive water intake
  • Nochronic kidney diseaseoracute kidney injury
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14
Q

What is an important complication of treating hyponatraemia?

A

Central pontine myelinolysis(CPM) is also (and more accurately) known as “osmotic demyelination syndrome”. It is usually a complication of long term severe hyponatraemia(< 120 mmols/l) being treated too quickly (> 10 mmol/l increase over 24 hours).

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15
Q

Dietary advice for a patient with CF?

A

High calorie, high fat, with pancreatic enzyme supplementation for every meal.

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16
Q

What are the genetics of fragile x?

A

X-linked on FMR gene
CGG repeat disorder.

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17
Q

What are the features of fragile x syndrome?

A

Long face, prominent forehead and chin, protruding ears, large testes, flat feet, mitral valve prolapse.

Autism and anxiety.

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18
Q

How should challenging behaviour and intellectual disability be assessed?

A
  • Developemental history
  • Response to previous interventions for challenging behaviour
  • Independent living skills / occupational ability
  • History of trauma / change in life events
  • Relationship with carers / family
  • Sensory profile
  • Environment
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19
Q

How should people with challenging behaviour be managed? OSCE

A

MDT
PBS (positive behavioural support)!!
Treat underlying health issues
Staff training and communication guidelines
Adapt environment
Establish diagnoses and prescribe psychotropic medication where appropriate.

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20
Q

What does PBS (positive behavioural support) aim to do?

A

Increase domestic activity skills, engagement and quality of life.

Increase community inclusion.

Improve physical health and management.

Preventative strategies to avoid the behaviour and reactive strategies during crisis.

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21
Q

Define challenging behaviour:

A

Behaviour can be described as challenging when it is of such an intensity, frequency or duration as to threaten the quality of life and or the physical safety of the individual or others and is likely to lead to responses that are restrictive, aversive or result in exclusion.

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22
Q

Investigations for someone presenting with challenging behaviour: OSCE

A

Abdo exam - to rule out constipation.

Sensory tests - hearing and sight.

Otoscopy to rule out infection.

Bloods - FBC (anaemia) U&E’s, LFT’s, TFT’s, Bone profile (hypocalcemia), B12.

Urine Dipstick - rule out UTI

H.pylori-causing pain

Dental check.

May consider a CT head if acute behavioural change.

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23
Q

What are the 5 principles when assessing capacity?

A
  • Principle 1: A presumption of capacity.
  • Principle 2: Individuals being supported to make their own decisions.
  • Principle 3: Unwise decisions.
  • Principle 4: Best interests.
  • Principle 5: Less restrictive option.
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24
Q

What is the two stage test of capacity and what criteria are tested to assess capacity?

A
  1. Does the person have an impairment of their mind or brain?
  2. Does the impairment mean the person is unable to make a specific decision when they need to?

The Mental Capacity Act 2005 states a person is unable to make a decision if they cannot

  1. Understand
  2. Retain
  3. Evaluate
  4. Communicate
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25
Q

Gold standard answer on how to manage challenging behaviour?

A

MDT and a PBS plan (positive behavioural support plan).

  • then break it down.
  • person centred value based approach.
  • Least restrictive option!
26
Q

What are the three main features of autism spectrum disorder?

A
  1. Abnormalities in reciprocal social interaction
  2. Abnormalities in social communication
  3. Restricted, stereotyped, repetitive behaviour

In addition, there also needs to be abnormal development prior to the age of three, e.g. delay in speech.

27
Q

When can anti-psychotic medication be prescribed for challenging behaviour?

A
  • Psychological or other interventions do not produce change in agreed time.
  • Treatment for co-existing mental or physical illness has not led to reduction in behaviour or:
  • The risk to the person or others is very severe (e.g. violence, aggression or self-injury).
28
Q

What medications are used to manage challenging behaviour?

A

Diazepam / risperidone

29
Q

What is STOMP?

A

Stopping the overprescribing of medication of people with a intellectual disability, autism or both.

Obstacles are:

  • Lack of funding from social services for activities. Frequent changes of staff or lack of consistency that may trigger challenging behaviour.
  • Inappropriate placements.
  • “Diagnostic overshadowing”
  • believing that the person’s symptoms are due to their intellectual disability or autism rather than a different cause, e.g. a physical or a mental illness.
  • Lack of appropriately skilled members of the intellectual disability team, e.g. no LD nurses / LD Psychiatrist / O. T / SALT / physiotherapist, or long waiting lists for psychology input.
30
Q

What are the three core features of depression?

A
  1. Low mood
  2. Anhedonia
  3. Anergia
31
Q

How should a diagnosis of depression be approached?

A
  1. Comprehensive history
  2. Exclude an organic cause: FBC, TFT’s, U&E’s, LFT’’s, B12, Folate, Bone profile, diabetes screen.
  3. Exclude any illicit substance use / medication related.
  4. Bipolar vs Unipolar depression?
  5. Symptoms present for at least 2 weeks.
32
Q

Read: Organic disease that can cause low mood:

A
  • Neurological disease such as Parkinson’s disease, dementia and multiple sclerosis
  • An endocrine disorder, particularly thyroid dysfunction and hypo/hyperadrenalism (e.g. Cushing’s and Addison’s disease)
  • Drugs (e.g. steroids, isotretinoin (roaccutane), alcohol, beta-blockers, benzodiazepines and methyldopa
  • Chronic conditions such as diabetes and obstructive sleep apnoea. Additionally, long-standing infections such as mononucleosis.
  • Neoplasms and cancers - pancreatic cancer is a notable example. However, low mood can theoretically be a presenting complaint in any cancer. It may be as a result of pro-inflammatory cytokines and immune system modulation.
33
Q

Explain the 1st line pharmacological therapy for depression:

A

Start with an SSRI (Sertraline, Fluoxetine, Citalopram) and assess within 2 weeks of initiation. Re-check after 4 weeks. Warn about suicidal thoughts in patients under 30. If no response try an alternative SSRI.

34
Q

How to manage a patient that has no response to an SSRI?

A
  1. Try a second SSRI
  2. If no response to a second SSRI try an SNRI (Venlafaxine).
    • Could also try Mitrazapine which helps with sleep and appetite disturbance.
  3. If no response then try in combination (SSRI+mitrazapine or Venlafaxine + mitrazapine).
35
Q

Why should trycyclic antidepressants be avoided when treating depression?

A

Cardiotoxic in overdose and poorly tolerated anyway.

36
Q

Short term side effects of ECT?

A

Short-term side effects of ECT can include headaches, muscle aches or pains, nausea, temporary memory loss, and confusion.

Due to the induced seizure, there is a risk of damage to the teeth or mouth, and due to the general anaesthetic, there is a small risk of death.

37
Q

Long term side effects of ECT?

A

Persistent memory loss.

38
Q

What medication is firstline for depression in children?

A

Fluoxetine

39
Q

Skim depression diagnosis:

A

Mild depression = 2 core features and 2 features

Moderate = 2 core and 3/4 other features

Severe = 3 core and 5 or more other features

Core symptoms:

  • Low mood
  • Anhedonia
  • Anergia

Other Features

  1. Depressed mood or irritable most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful).
  2. Decreased interest or pleasure (anhedonia) in most activities, most of each day
  3. Significant weight change (5%) or change in appetite
  4. Change in sleep: Insomnia or hypersomnia
  5. Change in activity: Psychomotor agitation or retardation
  6. Fatigueor loss of energy
  7. Guilt/worthlessness: Feelings of worthlessness or excessive or inappropriate guilt
  8. Concentration:diminished ability to think or concentrate, or more indecisiveness
  9. Suicidality:Thoughts of death or suicide, or has suicide plan.
40
Q

What is the management for acute bipolar disorder?

A

Generally olanzapine + fluoxetine.

(antipsychotic + antidepressant)

41
Q

1st line prophylaxis for patients with bipolar disorder?

A

Lithium carbonate or Depakote (sodium valproate)

42
Q

2nd line prophylaxis for patients with bipolar disorder?

A

Carbamazepine

43
Q

How to differentiate mania from hypomania?

A

The key differentiation is psychotic symptoms (e.g.delusions of grandeur or auditory hallucinations) which suggest mania.

Additionally, the DSM states that in hypomania “the episode (should not be) severe enough to cause marked impairment in social or occupational functioning, or to necessitate hospitalisation, and there are no psychotic features”.

44
Q

Most common cause of haemolytic uremic syndrome

A

The most common cause is Shiga-toxin producing Escherichia coli, particularly the O157:H7 strain.

45
Q

When should you consider HUS as a differential?

A

Normocytic anaemia, thrombocytopaenia and AKI following diarrhoeal illness - consider HUS
- may have diarrhoea + multiple petichae

46
Q

CF pseudomonas culture management in a stable patient

A

Oral ciprofloxacin is recommended and is combined with inhaled antibiotics for eradication.

47
Q

Eye discharge 0-12months most common cause

A

lacrimal immaturity

48
Q

Fever pain score criteria

A
  • Feverduring previous 24hours
  • P–Purulence (pus on tonsils)
  • A–Attended within 3days of the onset of symptoms
  • I–Inflamed tonsils (severely inflamed)
  • N–No cough or coryza
49
Q

Abx for otitis externa

A

Otitis externa in diabetics: treat with ciprofloxacin to coverPseudomonas. Fluclox normally.

50
Q

Gold standard framework

A

Framework for palliative care patients

51
Q

What is red on the GSF (palliative)?

A

Dying in days to weeks.

52
Q

What is amber on the GSF (palliative)?

A

1-6 months

53
Q

What is green on the GSF (palliative)?

A

6-12 months

54
Q

What cancers cause thrombocytosis? LEGOC

A

Lung cancer
Endometrial cancer
Gastric cancer
Oesophageal cancer
Colorectal cancer

55
Q

Initial screening test for hep c

A

HCV antibody

56
Q

Ramipril can cause what electrolyte abnormality

A

High K+

57
Q

Symptoms of high K+

A

Nausea
Muscle paralysis
Palpitations
Paraesthesia

58
Q

How long to continue contraception after menopause?

A

> 50yrs 12 months
< 50yrs 24 months

59
Q

Amitriptyline is used to treat which headaches?

A

MOH
Tension
Migraine

60
Q

What medication is recommended for fibromyalgia?

A

Dluoxetine