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Year 2 Revision > People and illness > Flashcards

People and illness Flashcards

1
Q

Define ADHD.

A

A developmental disorder characterized by grossly excessive levels of activity and a marked impairment of the ability to attend and concentrate.

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2
Q

Describe the clinical features of ADHD.

A

Inattention
Poor concentration - moves from one task to another
Excessive activity- disorganised, fidgety
Impulsivity - poor assessment of danger and accident prone, poor peer relationships.

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3
Q

Name the susceptibility genes associated with ADHD.

A 
DRD4 Receptor 7-Repeat Alleles
DAT1 – Dopamine Transporter gene
DRD5  - Dopamine receptor gene   
5HTT – Serotonin Transporter gene
HTR1B - Serotonin receptor gene
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4
Q

What is the link between genetics and environment in the development of ADHD.

A

Genetic factors contribute to the development of behavioural symptoms on a background of high environmental adversity.

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5
Q

Name some of the organic factors that contribute towards ADHD.

A

smaller brain volume – frontal & parietal cortex
smaller basal ganglia
right dorso-lateral prefrontal lobe reduced
smaller cerebellar vermis

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6
Q

List some of the co-morbidities associated with ADHD.

A 
Sleep disorders
ODD
OCD
Specific learning disabilities - i.e. dyslexia 
Dyspraxia 
Social communication difficulties 
Anxiety
Tourette syndrome 
Depression
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7
Q

How is ADHD assessed?

A 
no specific diagnostic test
direct observations in >1 setting
psychoeducational assessment
structured questionnaires 
Identifying co-morbidities 
developmental history
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8
Q

What additional tests should be performed in assessment of ADHD?

A

hearing and vision screening checks
screening for neurological signs and physical anomalies
Baseline height & weight (record on growth chart)
Baseline blood pressure and heart sounds

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9
Q

What is the mechanism of action of psychostimulants in the treatment of ADHD? Give two examples of this type of drug.

A

Acts on D1 receptors in the prefrontal cortex and D2 in the striatum.
Methylphenidate (Ritalin)
Dexamphetamine

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10
Q

What is the mechanism of action of Atomoxetine in the treatment of ADHD?

A

Noradrenaline reuptake inhibitor. Enhances transmission of Noradrenaline in the prefrontal cortex.

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11
Q

What type of drug is Clonidine and what condition is it used to treat?

A

alpha-2 adrenergic receptor agonist

ADHD

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12
Q

What type of drug is Guanfacine and what condition is it used to treat?

A

alpha2A adrenergic receptor agonist

ADHD

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13
Q

What are some of the side effects of psychostimulants as a treatment for ADHD?

A

Impaired growth (not normally long term)
Difficulty sleeping.
Anorexia
HR and BP abnormalities

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14
Q

How long does it take for Atomoxetine to take effect as a treatment for ADHD?

A

About 4-6 weeks.

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15
Q

What are some of the side effects of using Guanfacine as a treatment for ADHD?

A

Weight gain, tiredness, dizziness, hypotension.

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16
Q

List some of the different forms of dexamphetamine available.

A

Elvanse - long acting
Daytrana - transdermal patch
Dexedrine - fast acting 5mg tablets

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17
Q

How should health be monitored in children on psychostimulants?

A

HR and BP on every dose adjustment and every 6 months
Pre-treatment height and weight and every 6 months
Complete detailed history

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18
Q

What are some contraindications to using psychostimulants?

A

History of depression, anorexia, psychosis, suicidal tendencies, preexisting cardiovascular disorders.

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19
Q

What should be monitored in children who taken Atomoxetine?

A

BP, HR, height, weight, mood, LFTs.

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20
Q

What are some of the side effects of Atomoxetine?

A

Reduced sleep, reduced apatite, suicidal ideation.

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21
Q

How does clonidine and guanfacine work in the treatment of ADHD?

A

Inhibit noradrenaline at the synapse.

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22
Q

How long does it take clonidine and guanfacine to have a therapeutic effect?

A

4-6 weeks

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23
Q

Name some of the non-pharmacological treatments of ADHD.

A

Pyschoeducation
Behaviour therapy
Cognitive behavioural therapy (CBT)
Parent education programmes

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24
Q

What dietary changes can be made to treat children with ADHD?

A

Reducing sugar, additives, caffeine, food colourings.

Supplement diet with omega-3 and omega-6 fatty acids,

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25
Q

What are the 7 categories to be explored in a mental state exam?

A 
 Appearance & Behaviour
 Speech
 Mood & Affect
 Thought Form & Content
 Perception
 Cognition
 Insight
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26
Q

What would you include in assessment of appearance as part of MSE?

A

Ethnicity, build, hair colour, clothing.
Biological vs chronological age
Evidence of self-neglect
Physical illness or intoxication

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27
Q

What would you include in assessment of behaviour as part of MSE?

A

Level of motor activity (agitation or motor retardation)
Eye contact
Rapport and engagement with interview
Body language and posture
Any unusual or socially inappropriate behaviour.

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28
Q

What would you include in assessment of speech as part of MSE?

A 
Rate and quantity of speech
Rhythm
Volume
Tone 
Spontaneity
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29
Q

Define mood and effect.

A

Mood: a person’s emotional state overall.
Affect: changes in a person’s emotions that you observe moment to moment during the interview.

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30
Q

How would you assess a person’s subjective and objective mood?

A

Subjective: how the person tells you how they feel in their own words.
Objective: your impression of the person’s mood during the interview. (euthymic (normal), elevated, low, anxious).

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31
Q

Define the following words which describe effect: reactive, flattened, blunted, labile.

A

Reactive: appropriate to the situation or topic being discussed.
Flattened: limited emotional reaction.
Blunted: no observed emotional reactions (specifically associated with psychosis)
Labile: excessive emotional fluctuations.

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32
Q

What would you include in assessment of thought form as part of MSE?

A

Is the flow of their thoughts logical or illogical.

Include specific quotes if possible.

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33
Q

Define the terms “flight of ideas” and “knight’s move thinking”. What conditions are these terms associated with?

A

“flight of ideas” - rapid flow of speech, moving from topic to topic with logical connections (mania)
“knight’s move thinking” - little or no logical connections between thoughts (schizophrenia)

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34
Q

What would you look for when you assess thought content as part of a MSE?

A

Are there any topics discussed more than others?

Delusions, over-valued ideas and obsessions.

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35
Q

Define delusions, over-valued ideas and obsessions. What conditions are associated with these terms?

A

Delusions: a fixed false belief that is held in contrary to evidence that is out of keeping with the person’s religious or cultural background (psychosis)
Over-valued idea: a false belief, not totally fixed but causing great disability. (Anorexia nervosa, hypochondriasis)
Obsessions: recurrent, intrusive, distressing ideas, impulses or images that the patient recognises as their own (OCD)

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36
Q

What must ALWAYS be included in a mental state exam?

A

Risk assessment - any thoughts of harm to self or others, including degree of planning and intent. Always document, even if negative.

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37
Q

What should you look out for when assessing a person’s perception as part of a MSE?

A

Hallucinations - perception without external stimulus.

Illusion - false perception of a real stimulus (e.g. seeing a person in a shadow)

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38
Q

What conditions are associated with auditory hallucinations and visual, olfactory, gustatory and tactile hallucinations?

A

Auditory - psychosis

All the others - not associated with pychiatric illness - drugs, drug or alcohol withdrawal, delirium.

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39
Q

How would you assess alertness, orientation, concentration and memory as part of the cognition section of a MSE?

A

Alertness - do they seem fully awake.
Orientation - to time, place and person.
Concentration - can they maintain focus during the interview, are they easily distracted.
Memory - tell them 3 objects, ask to repeat until they are correct, continue with history and ask again in a few minutes.

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40
Q

Define insight as part of a MSE.

A

The patient’s understanding of their presentation and need for treatment.

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41
Q

Define psychiatry.

A

Medical specialty concerned with diagnosis, treatment and prevention of mental health disorders

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42
Q

Define psychosis.

A

A mental illness characterized by an altered relationship with reality.

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43
Q

Define bipolar disorder.

A

Mental disorder characterized by periods of depression and mania.

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44
Q

Describe the aetiology of depression in basic terms.

A

Combination of biological, psychological and social factors.

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45
Q

Describe the biological factors which cause depression.

A

Genetics
Medical comorbidities (thyroid, MS)
Psychiatric comorbidities (schizophrenia, OH)
Medications (steroids)
Neurochemical (decreased 5HT, NA, DA)
Neuroendocrine (decreased T3, TSH, increased cortisol)

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46
Q

Describe the psychological factors which cause depression.

A

Personality traits - anxious, obsessive
Personality disorders
Coping skills
Adverse life events

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47
Q

Describe the social factors which cause depression.

A

Poor social support
Socioeconomic disadvantage
Northernization

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48
Q

What is the point prevalence and the lifetime incidence of depression? What percent of people never seek treatment for depression?

A

Point prevalence 4-7%
Lifetime incidence 20%
33% never seek treatment

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49
Q

What are the core clinical features of depression?

A

Low mood +/- anhedonia +/- fatigue, every day >2 weeks

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50
Q

What are the biological clinical features of depression?

A

Diurnal variation (worse in the morning), insomnia, ↓ appetite,↓ weight, ↓ libido, constipation, amenorrhoea

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51
Q

What are the cognitive clinical features of depression?

A

↓ concentration, slow / negative thinking, guilt, loss of self esteem, hopeless, suicidality

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52
Q

How is mild, moderate and severe depression classified?

A

Mild: 2 or more core features + 2 or more associated features + ok function
Moderate: 2 or more core, 4 or more associated, low function
Severe: 2 or more core, 6 or more associated, very low function +/- psychosis

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53
Q

What are some of the potential outcomes of depression?

A 
Recurrent depressive disorder 
Substance misuse 
Anxiety 
Suicide 
Cardiovascular disease
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54
Q

What are some possible differential diagnoses of depression?

A

Dysthymia - low mood, chronic >2 years but not enough for depression
Cyclothymia - alternating mild low and elevated mood.
Atypical depression - low mood but reversed associated side effects.
Seasonal affective disorder - winter
Adjustment reaction - adaptation to stressor, can include low mood.
Grief - feelings, thoughts and behaviour associated with bereavement.

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55
Q

How is depression assessed?

A 
Clinical history
Risk assessment
MSE (mental state exam)
Physical exam
Baseline blds
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56
Q

When can be depression be life threatening? How is this managed?

A

If the person is suicidal or due to self neglect (i.e. not eating and drinking)
Needs hospitalization. If they refuse, needs the mental health act.

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57
Q

What type of treatment would be used from moderate and severe depression?

A

Moderate: antidepressants
Severe: antidepressants + antipsychotics, electroconvulsive therapy (ECT)

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58
Q

How do SSRIs work in treating depression? How long do they take to have an effect? Give a few examples.

A

Block 5HT reuptake, increasing the amount in the synapse and magnifying its effect. 4-5 weeks. Citalopram, fluoxetine.

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59
Q

What are the side-effects of SSRIs?

A

Nausea, vomiting, weight gain, dizziness, anxiety, suicidality, mania.

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60
Q

How to tricyclic antidepressants (TCA) work? What are some of the side-effects? Name some examples.

A

Block 5HT reuptake, NA uptake.
Side effects: anti-adrenergic (↓BP), anti-cholinergic, ECG changes (arrhythmia).
Amitriptyline, maprotiline.

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61
Q

How do monoamine oxidase inhibitors (MAOIs) work in the treatment of depression? What are some of the side-effects?

A

They block MAO-A and MAO-B which break down 5HT, NA and DA in the CNS.
Hypertension.

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62
Q

What are the 1st, 2nd and 3rd line pharmacological treatments for depression?

A

1st - SSRI
2nd - TCA
3rd - MAOI

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63
Q

What is electrotherapy and what conditions can it be used to treat? What are the risks and side-effects?

A

Controlled seizure and anaesthetic used to treat depression, mania and catatonia.
Anaesthetic risks and side effects: memory (rare).

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64
Q

How can depression be treated psychologically?

A

CBT
Psychotherapy
Family therapy

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65
Q

What can be targeted as part of a social approach to treating depression.

A

Activities, housing, finances, employment.

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66
Q

What are the normal stages of grief?

A 
Denial
Anger 
Bargaining 
Depression
Acceptance
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67
Q

Describe the elimination of nascent cancer.

A
  1. Innate immune response recognises tumour cell establishment.
  2. Natural Killer cells and other effectors recruited to site by chemokines, which also target tumour growth directly.
  3. Tumour specific T cells home to tumour site, along with macrophages and other effectors to eliminate tumour cells.
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68
Q

What is immunoediting? What factors allow for immunoediting to occur?

A

The production of low antigenicity tumour cells by selection.
Pressure from immune system coupled with genomic instability.

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69
Q

What factor will be increased to allow neovascularisation of a tumour to occur?

A

increased VEGF

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70
Q

What factors need to be increased for intravasation of a tumour to occur?

A

Increased MMPs and uPA (urokinase plasminogen activator).

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71
Q

A change in what factors needs to occur for extravasation of a tumour to occur?

A

Change in selectin and CDD4

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72
Q

What factor need to be increased, decreased and changed for local invasion of a tumour to occur?

A

Increased - HGF, CKs, uPA, MMPs, CKR
Decreased - E-cadherins
Changed - integrins

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73
Q

What factor needs to be decreased for growth at the ectopic site to occur?

A

Decreased angiostatin/endostatin which is an anti-angiogenic factor.

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74
Q

What is the result of a mutation in the oncogene that encodes BRAF?

A

Leads to constitutive activation of downstream signalling in the MAP kinase pathway. Uncontrolled cell proliferation.

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75
Q

How does vemurafenib work in the treatment of people whose metastatic melanoma has a BRAF gene change?

A

It is a reversible ATP competitive inhibitor which binds to the kinase domain of BRAF. Causes programmed cell death of the tumour cells.

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76
Q

How does nivolumab work in the treatment of cancer?

A

Binds to PDL-1, preventing it from binding to the PD-1 domain on T cells, stopping T cells from being destroyed.

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77
Q

How does IL-2 work in treating cancer? What precautions have to be taken when using IL-2 therapy?

A

Promotes expansion of tumour specific T cells. Has a very narrow therapeutic index, must be administered by a doctor who has a license to administer IL-2.

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78
Q

What type of drug is ipilimumab? How can it be used to treat cancer? What are potential adverse effects?

A

Monoclonal antibody. CTLA-4 is an ‘off-switch’ for cytotoxic T cells. CTLA-4 is often upregulated by tumour cells. Ipilimumab blocks CTLA-4, enhancing inflammation and blocking immunosuppressive effects. It also increases the number of active T cells.
Gut blisters.

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79
Q

Name the different primary and secondary lymphoid organs?

A

Primary: the thymus
Secondary: Lymph nodes, the spleen, tonsils, peyer’s patches and mucosa associated lymphoid tissue (MALT)

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80
Q

Where are T cells and B cells produced and programmed?

A

B cells - produced and programmed in the bone marrow.

T-cells - Produced in the bone marrow, programmed in the thymus.

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81
Q

What is Di George syndrome?

A

When someone is born without a thymus therefore no T cells are programmed and so no cell mediated immunity.

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82
Q

Where do B-cells get their name?

A

Named after the bursa of fabricius, an organ in birds where B-cells are produced.

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83
Q

What is the name given to the first node that a lymphatic vessel drains into?

A

The first regional lymph node.

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84
Q

What is lymphoid tissue?

A

Tissue consisting of a large collection of small lymphocytes (7micrometers) held together by a delicate skeleton of reticular fibres.

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85
Q

By what two processes are lymph nodes cleaned?

A

1) mechanical filtration - settling tank

2) biological filtration - via star shaped macrophages called fixed stellate macrophages.

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86
Q

What kind of epithelium are tonsillar crypts lined with?

A

Stratified squamous epithelium.

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87
Q

In the appendix, where is the bulk of the lymphoid tissue located?

A

In the submucosa.

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88
Q

In the spleen, where are B-cells and T-cells located?

A

T cells around the arteries, B cells further out.

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89
Q

How are old RBCs removed in the spleen?

A

They are phagocytosed by macrophages.

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90
Q

In the thymus, what type of cells surround the developing T cells and bring about maturation?

A

Thymic nurse cells.

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91
Q

In a lymph node, what does the presence of lymphoid nodules in the outer cortex suggest?

A

That an antibody response has occurred.

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92
Q

What do lymphoid nodules produce?

A

Memory B lymphocytes.

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93
Q

Where are B cells and T cells located in a lymph node?

A

B-cells - outer cortex and in the medullary cords.

T-cells - deep cortex

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94
Q

What type of drug is nivolumab? How does it work as a cancer treatment?

A

A monoclonal antibody. It blocks PDL-1 on tumour cells, preventing the activation of PD-1 on T-cells, preventing apoptotic destruction of T-cells.

95
Q

Name some different cell-based cancer treatments.

A 
Haemopoetic stem cells
Tumour infiltrating T-cells
Dentritic cell vaccines
NK cells
Gamma-delta cells
Virus specific T cells
Genetically engineered T cells
96
Q

Name three angiogenesis inhibitors used in cancer treatment. What type of drugs are these?

A

Sunitinib
Pazopanib
Axitinib

Kinase inhibitors

97
Q

What are the advantages of using new targeted therapies to treat cancer?

A

Targeted to cancer cells so less effects on normal cells. This means fewer side effects, allowing you to use higher doses which means potentially better therapeutic effect.

98
Q

What is the defining lesion of chronic myeloid leukaemia?

A

BCR-abl translocation.

99
Q

How does a BCR-abl translocation cause cancer?

A

abl is a ATP dependent kinase which causes cell proliferation. It is normally tightly regulated. BCR is permanently switched on and when bound to abl it causes uncontrolled proliferation.

100
Q

What type of drug is imatinib? How does it work to treat cancer? What cancer would it be used to treat?

A

Tyrosine kinase inhibitor. Drug binds to abl in place of ATP and switches it off, preventing uncontrolled proliferation. Chronic myeloid leukaemia.

101
Q

What is targeted therapy in cancer?

A

Drugs which target a specific process in an aberrant molecular pathway.

102
Q

In kidney cancer, how does a mutation in VHL result in angiogenesis?

A

VHL normally keeps HIF in check. When VHL is mutated, HIF allows angiogenesis to occur uninhibited.

103
Q

Name three different mutations in which tyrosine kinase inhibitors can be used as treatment.

A

Raf kinase mutations in melanoma
MAP kinase in melanoma
Her2 in breast cancer

104
Q

In what type of cancer would castration be a first line treatment? What different methods of castration can be used?

A 
Metastatic prostate cancer. 
GnRH agonists (overdrive pathway and switch it off)
GnRH antagonists
Estrogens
AR (androgen receptor) antagonists
105
Q

What are some of the barriers to targeted therapy?

A

The drugs don’t work in cancers where there is a mutated tumour suppressor gene.
Cancer cells are always mutating and can eventually become resistant to the drugs.

106
Q

Describe personalised/precision medicine.

A

Doing a test to determine which patients will respond to which drug and only treating the patients with the drugs that they will respond to.

107
Q

What is the difference between predictive markers and prognostic markers?

A

Predictive markers predict which patients will benefit from specific treatment and helps choose which drug to use.
Prognostic markers inform about outcome regardless of treatment. Helps you choose which patients to treat but not how to treat them.

108
Q

What are some of the problems associated with precision medicine?

A

There is no targeted drug for most patients.
Caner usually isn’t a single mutation disease. Within a tumour you may have different parts with different mutations.
Requires biopsies which are difficult to get.

109
Q

What cancer is Enzalutamide used to treat? How does it work?

A

Prostate cancer. Enzalutamide is an AR signalling inhibitor.

110
Q

What has been the percentage increase in discharges with alcoholic liver disease between 2000/1 and 2009/10?

A

> 60% increase

111
Q

What has been the percentage increase in alcohol related deaths between 1980 and 2010?

A

222% increase

112
Q

Heavy drinking results in excess of what byproduct of alcohol metabolism?

A

Reactive Oxygen Species

113
Q

Explain how portal circulation endotoxaemia occurs? How does this result in liver injury?

A

Increased permeability leads to translocation of gut bacteria into the portal venous system.
Promotes activation of kupffer cells which produce TNF-alpha, causing inflammation.

114
Q

Describe some of the features of alcohol dependency.

A

Alcohol tolerance, withdrawal symptoms, persistent unsuccessful attempts to cut down, inability to function normally without alcohol, morning drinking, inability to drink to a limit, organizing the day around drinking, trembling after drinking.

115
Q

Describe some of the physical and psychological symptoms associated with alcohol withdrawal.

A

Sweating, nausea, tremors, visual hallucinations, seizures (extreme)
Depression, anxiety, insomnia, irritability, restlessness.

116
Q

Describe some of the social effects of alcohol and drug dependence on the individual, family and society.

A

Individual - unemployment, financial difficulties, increased risk taking behaviour - accidents, injuries, pregnancy, STIs.
Family - marital breakdown, domestic violence, child abuse/neglect
Society - violence, crime, homelessness, huge financial burden on the NHS.

117
Q

Describe some of the psychological effects of alcohol.

A

Depression, anxiety, suicide/attempted suicide, pathological jealousy.

118
Q

What physical conditions can be caused by harmful use of alcohol?

A

Acute gastritis, pancreatitis, liver disease, diabetes, cancer (bowel, breast, laryngeal, pharyngeal, oesophageal, liver, mouth.)

Hypertension, cardiomyopathy, arrhythmias, coronary heart disease, tachycardia.

Wernicke-korsakoff syndrome, alcoholic cerebellar degeneration, alcohol related dementia.

Acute and chronic myopathy, immune system effects- more susceptible to infection.

119
Q

What is the legal alcohol limits in breath, blood and urine for driving in Scotland?

A

Breath - 22mg/100ml
Blood - 50mg/100ml
Urine - 67mg/100ml

120
Q

What are the legal consequences for driving above the legal limit in Scotland?

A

6 months imprisonment
Unlimited fine
Driving ban for 1 year (3 years if convicted twice in 10 years)

121
Q

What is the recommended weekly drinking limits for men and women? Is it best to spread this out through the week or consume in one sitting?

A

No more than 14 units of alcohol per week. Best to spread out over three or more days.

122
Q

What are the symptoms of delirium tremens? How does this differ from the symptoms of alcohol withdrawal?

A

Confusion, hallucinations, severe agitation, delusions, seizures, tachycardia, sweating, hypertension, tremor, ataxia.
Differs because with DT you have altered mental state - patient will be confused.

123
Q

How long does it typically take for delirium tremens to set in after drinking is stopped/reduced?

A

24-72 hours

124
Q

What can drinking during pregnancy increase your risks of?

A

miscarriage, prematurity, low birth weight, foetal alcohol syndrome (FAS)

125
Q

Describe the clinical features of foetal alcohol syndrome.

A

Facial abnormalities - microcephaly, flat philtrum, lowered nasal bridge, epicanthal folds, micrognathia (small chin), thin upper lip, minor ear abnormalities, small palpebral fissures.

Learning difficulties, hyperactivity, balance problems.

126
Q

List some of the non-pharmacological treatments of alcohol dependence.

A

BRIEF intervention
CBT
Self-help groups - Alcoholics Anonymous
Family therapy

127
Q

List some of the medications (+ doses) that can be used to manage withdrawal symptoms.

A

Diazepam - orally 10-20mg
Chlordiazepoxide - orally 30-60mg
Benzodiazepine - only if symptoms not controlled with the others. Not to be given in patient still drinking.

128
Q

List some of the drugs which can be used to treat alcohol dependence and how they work.

A

Naltrexone - opiod antagonist, reduces relapse into heavy drinking.
Acamprostate - acts on GABA receptors, reduces alcohol cravings.
Disulfiram - has unpleasant reaction with alcohol, stops people wanting to drink.

129
Q

Lack of what vitamin causes wernicke-korsakoff syndrome? How can this syndrome be prevented?

A

Thiamine

Indentifying those at risk of WK sydrome and giving them oral thiamine (300mg/day)

130
Q

Briefly describe the main mechanism of alcohol metabolism in the body.

A

Alcohol is converted to acetaldehyde in the cytosol by alcohol dehydrogenase (ADH).
Acetaldehyde is converted to acetate in the mitochondria by acetaldehyde dehydrogenase (ALDH).

131
Q

If the central mechanism of alcohol metabolism is flooded, what other mechanisms are used? What byproduct is produced by these alternative pathways?

A

MEOS: microsomal ethanol oxidising system

or

Catalase reactionw whick occurs in the peroxisomes.

Reactive oxygen species (ROS)

132
Q

Describe the intrinsic pathway of apoptosis in Alcohol-related liver disease (ALD)?

A
  1. initiated by oxidative stress
  2. leads to leakage of pro-apoptotic factors from mitochondia i.e. cytochrome C
  3. Pro-apoptotic factors lead to activation of caspases.
133
Q

Describe the extrinsic pathway of apoptosis in Alcohol-related liver disease (ALD)?

A
  1. initiated by TNF-alpha

2. binding to TNF receptors leads to caspase activation via FADD and TRADD.

134
Q

Describe the difference between apoptosis and necrosis.

A

Apoptosis - requires energy, natural cell death, stimulated by cell signals, benefical, cell fragments sends signals that initiate phagocytosis.
Necrosis - no energy required, traumatic cell death, stimulated by other factors, cannot send signals so cell debris builds up.

135
Q

How does malnutrition exacerbate alcohol related illness?

A

Depletion of trace elements i.e. zinc may exacerbate ROS production and promote apoptosis.
Vitamin deficiency may lead to impaired metabolism of methionine and reduction in glutathione.

136
Q

What are the consequences of disrupted methionine metabolism?

A

Apoptosis
Inflammation
Oxidative stress

137
Q

How does obesity exacerbate ALD?

A
  • Alcohol induces a lipdystrophy - less peripheral fat, more visceral fat.
  • induction of CYP2E1, increasing ROS
  • obesity induces pro-inflammatory state.
138
Q

Describe the pathological spectrum of ALD.

A

Normal liver > steatosis > steatohepatitis > fibrosis > cirrhosis > hepatocellular carcinoma.

139
Q

How can cirrhosis be diagnosed?

A

Transient elastography. In a normal liver speed of return is slow. In a fibrotic liver, speed of return is quick.

140
Q

How does alcoholic liver disease affect liver function tests?

A

Raised AST:ALT ratio
AST<500, ALT usually <300
Alcoholic hepatitis may appear cholestatic.

141
Q

What are the characteristic features of alcoholic hepatitis?

A

Hepatomegaly, fever, leucocytosis, hepatic bruit

142
Q

What are the essential features required to diagnose alcoholic hepatitis?

A 
Recent excess alcohol
Bilirubin>80micromol/l
Exclusion of other liver disease
AST<500
AST:ALT ratio>1.5
143
Q

What scale is used assess severity of alcoholic liver disease?

A

The Glasgow Alcoholic Hepatitis Score (GAHS)

144
Q

How is alcoholic hepatitis treated? Patients with what GAHS have the greatest survival benefit?

A

Corticosteroids i.e. pregnisolone

GAHS≥9

145
Q

List some signs of chronic liver disease?

A

Spider naevi, foetor, encephalpathy, prolonged prothrombin time, hypoalbuminaemia

146
Q

List some signs of portal hypertension.

A

Caput medusa
Splenomegaly
Thrombocytopenia (low platelets)

147
Q

How is the severity of chronic liver disease assessed? What numerical scores would be considered mild, moderate, severe?

A

The childs-turcotte-pugh score:
Grade A: 5-6, mild
Grade B: 7-9, moderate
Grade C: 10-15, severe

148
Q

What are some of the clinical features of advanced liver disease?

A

Variceal haemorrhage, hepatic encephalopathy, ascites, hepatorenal failure, hepatocellular carcinoma.

149
Q

What is the strongest single predictor of suicide?

A

Alcohol

150
Q

What important the determinants of alcohol epidemics?

A

Cost and availability of alcohol.

151
Q

What are the effects on the CNS of chronic heavy drinking?

A

Neuropathies, cerebellar degeneration, dementia, wernicke-korsakoff’s syndrome

152
Q

What proportion of those who complete suicide were intoxicated with alcohol at the time?

A

4/5ths

153
Q

What is the current mortality rate for patients with DT? What are the most common conditions leading to death in DT patients?

A

5-15%

Respiratory failure and cardiac arrhythmias

154
Q

What factors contribute to alcohol problems?

A

Price and availability of alcohol
Genetics
Socio-economic factors
Cultural influence

155
Q

What are some of the psychiatric associations of opiate dependence?

A

Depression, attempted suicide/suicide, personality disorder, PTSD

156
Q

Benzodiazepine use is commonly associated with dependence on what class of illicit drugs?

A

Opiates

157
Q

What psychiatric problems are commonly associated with stimulant drugs?

A

Anxiety, depression, anti-social behaviour, paranoid psychosis.

158
Q

What are some predisposing factors to Wernicke-Korsakoff’s syndrome?

A 
Genetic predisposition to alcohol induced neurotoxicity
Quantity and frequency of alcohol use 
Severity of dependence
Withdrawal syndromes 
Other drug use
Concurrent liver damage

Weight loss in the past year
High Carbohydrate intake
Recurrent vomiting episodes

159
Q

What is an adults daily requirement of thiamine?

A

1-2mg

160
Q

What are the signs of Wernicke-Korsakoff syndrome?

A

Confusion
Eye-symptoms - gaze paralysis and nystagmus
Gait ataxia

161
Q

What areas of the brain are affected in Wernicke-Korsakoff’s syndrome?

A

Dorso-medial nucleus and mamillary bodies

162
Q

Describe korsakoff syndrome.

A

Prominent loss of recent memory.
Disturbances of time sense and ordering of events.
Difficulty learning new material.
Confabulation may be present. (unintentionally fabricated memories)
Other cognitive functions usually well preserved.

163
Q

What two brain structures can shrink as a long term effect of heavy drinking?

A

Ventricles

Cerebellum

164
Q

What are the two main aetiologies of Wernicke-korsakoff syndrome?

A

Alcohol neurotoxicity

Thiamine deficiency

165
Q

What two biochemical factors are important in the pathogenesis of hepatic encephalopathy?

A

Ammonia and the glutamate-glutamine cycle

166
Q

Define delirium.

A

Delirium is an acute, fluctuating change in mental status, with inattention, disorganised thinking, and altered levels of consciousness.

167
Q

Name some factors that predispose you to delirium.

A 
Older age
Cognitive impairment
Physical co-morbidity (i.e. cancer)
Psychiatric co-morbidity (i.e. depression)
Sensory impairment (vision, hearing)
Functional dependence (for mobility)
Dehydration/malnutrition
Drugs
Alcohol dependence
168
Q

Name some factors that precipitate delirium. Include metabolic factors, infection, medication, vascular, physical/psychological stress.

A

Metabolic - malnutrition, dehydration, anaemia, hypoxia, hypercapnoea, hypoglycaemia
Infection - especially UTI and resp.
Medication - Anticholinergics, opiods, dopaminergics, stetoids
Vascular - stroke, MI
Physical/psychological stress - urinary retention, severe constipation, chronic illness, traumatic event i.e. fracture

169
Q

What 4 features must a patient have to be diagnosed with delirium?

A
  1. A disturbance in attention (i.e. reduced clarity of awareness of environment)
  2. A change in cognition (i.e. memory disturbance, disorientation, language disturbance)
  3. Acute onset, different from baseline, fluctuates during course of the day.
  4. Disturbance caused by physiological consequences of a general medical condition.
170
Q

What are the symptoms of dementia?

A 
Memory loss
Cognitive impairment
Language  problems
Visuospatial  function
Impairment  of  intellectual ability
Personality  changes
171
Q

Describe the differences between dementia and delirium

A

Delirium: acute onset, fluctuating conscious level, underlying medical cause, disordered thinking, visual/tactile hallucinations, illusions.
Dementia: progressive, no alteration in consciousness, primary CNS disease, lack of insight, memory impairment, cognitive impairment.

172
Q

What is the prevalence of dementia in >65s and >85s?

A

> 65 - 10%

>85 - 40%

173
Q

What the clinical features of Alzheimer’s disease?

A

Memory impairment
Cognitive decline - language, writing, reading, calculation
Personality/mood changes
Neurological:
-frontal executive function - impairment of organizing, planning and sequencing.
- parietal presentation - visuospatial difficulties

174
Q

What are the main different types of dementia?

A

Alzheimer’s disease
Vascular dementia
Dementia with Lewy Bodies (DLB)
Fronto-temporal dementia

175
Q

Describe the changes seen in the behaviour of a patient with Alzheimer’s disease as it progresses from mild to severe.

A

Mild - memory loss, confusion, trouble handling money, poor judgement, mood changes, anxiety.
Moderate - Increased memory problems and confusion, difficulty recognising people, difficulty with language, restlessness, agitation, wandering and repetitive statements.
Severe - Weight loss, seizures, increased sleeping, loss of bladder and bowel control, loss of speech.
Death due to pneumonia.

176
Q

Describe the pathological changes in the brain of an Alzheimer’s disease patient.

A

Changes begin in the entorhinal cortex and hippocampus.
The cerebral cortex shrinks and ventricles enlarge.
Deposition of beta-amyloid in amyloid plaques in the cortex. Tau containing intracellular neurofibrillary tangles.

177
Q

What is vascular dementia (multi-infarct dementia)?

A

Reduced blood supply to the brain because of a series of mini strokes leading to damage and dementia.

178
Q

What are the two main features of neurodegenerative disease?

A
  1. Neuronal death

2. Systematic loss (symmetrical)

179
Q

Which parts of the brain show degeneration in the following conditions: AD, FTD, parkinson’s, huntington’s, ataxia?

A

Cortex: AD, FTD
Basal ganglia: Parkinson’s and Huntington’s
Cerebellum and spinal cord: ataxia

180
Q

Name some neurodegenerative diseases that are often/always genetic.

A

Huntington’s disease - always frontotemporal dementia - often
cerebellar ataxia - often

181
Q

Name some neurodegenerative diseases that often/always come about sporadically.

A

AD

Parkinson’s

182
Q

What mnemonic can be used to remember the potential differential diagnosis of a dementia like presentation?

A

AVDEMENTIA

Alzheimer Disease
Vascular Disease
Drugs, Depression, Delirium
Ethanol
Metabolic
Endocrine (thyroid, diabetes)
Neurologic (other dementia’s e.g Lewy body dementia)
Tumour, Toxin, Trauma
Infection
Autoimmune
183
Q

Name some of the reversible causes of dementia.

A 
Hypothyroidism
Normal pressure hydrocephalus
Drugs (opiates, sedatives, anticholinergics)
Tumours (eg meningioma)
Neurosyphilis
Chronic subdural haematoma
Whipple’s disease
Nutritional eg: Pellagra (VitB3 deficiency)
Psychiatric disorders
184
Q

What is the typical time of survival for someone who receives an Alzheimer’s disease diagnosis?

A

6-12 years

185
Q

Describe what would be seen in a macroscopic examination of the brain of a patient with severe AD.

A

Reduced weight
Cortical atrophy - sulcal widening and gyral atrophy
Thinned neocortical ribbon
Loss of white matter - hydrocephalus ex vacuo

186
Q

What are the risk factors for AD?

A 
Increasing age
Genetics - APP, presenilin, APOE4
Down's syndrome
Female gender
Head injury
187
Q

What are the risk factors for vascular dementia?

A

Underlying vascular pathology
Hypertensive
Vascular risk factors

188
Q

Describe the features of vascular dementia.

A

Evidence of cerebrovascular events
Memory impairment
Stepwise progression
Lack of insight

189
Q

Describe the macroscopic examination of the brain of a patient with vascular dementia.

A 
normal weight
No significant fronto-temporal atrophy
Mild/mod basal vessel atheroma (plaque)
Multiple areas of cystic disruption throughout cortex
Mild ventriculomegaly
190
Q

Describe the clinical features of a patient with dementia with Lewy Bodies.

A

Progressive cognitive decline
Fluctuating consciousness
Visual hallucinations
Parkinsonism

191
Q

Describe the pathological features of the brain of a patient with dementia with Lewy Bodies.

A

Similar features to AD and PD
Pallor of brainstem pigmented nuclei
Cortical Lewy bodies

192
Q

Abnormal aggregation of what protein is associated with Parkinson’s disease and dementia with Lewy bodies.

A

α-synuclein

193
Q

What is the difference between dementia with lewy bodies and Parkinson’s disease in terms of lewy body pathology and its clinical effect?

A

Lewy body pathology:
Parkinson’s - its of the nigrostriatal system
Dementia with lewy bodies - its of the cerebral cortex
Clinical effects:
Parkinson’s - extrapyramidal movement disorder
Dementia with lewy bodies - dementia

194
Q

What are the pathological and clinical features of dementia?

A

Clinical - cognitive and memory impairment, frontal lobe dysfunction (i.e. behaviour/personality changes, disinhibition, depression, agitation.
Pathological - Tau accumulation causing Pick’s bodies

195
Q

Which amino acid does transcription always start with?

A

Methionine

196
Q

Which of the following post translational modifications targets the protein for destruction?

A

Ubiquitination

197
Q

Which types of proteins undergo lysosomal degradation?

A

Proteins with a long half-life
Membrane proteins
Extracellular proteins

198
Q

Which types of proteins undergo proteosomal degradation?

A

Proteins with a short half-life
Key metabolic enzymes
Defective proteins

199
Q

Name some different processes involved in proteostasis.

A

Synthesis, folding, assembly, trafficking, degradation

200
Q

What type of bonds are responsible for secondary structure of proteins?

A

Hydrogen bonds between O and H atoms on different amino acids.

201
Q

What types of bonds are responsible for tertiary structure of proteins?

A

Hydrophobic interactions between non-polar R groups
Hydrogen bonds between polar R groups
Disulfide bonds

202
Q

What is a molecular chaperone?

A

Any protein that interacts with, stabilises or helps another protein to acquire its functionally active conformation, without being present in its final structure.

203
Q

What percent of newly folded proteins are misfolded?

A

30%

204
Q

Name a molecular chaperone that assists in folding and quality control of glycoproteins in the ER.

A

Calnexin

205
Q

Where are proteasomes located in a cell?

A

Cytosol and nucleus.

206
Q

What is the structure of a proteasome and what components make it up?

A

Hollow cylindrical structures made up of alpha and beta subunits and a CAP at the top and bottom.

207
Q

Describe the steps of proteasomal degradation.

A
  1. polyubiquitination
  2. polyUb-protein recognised by CAP
  3. polyUb removed; protein unfolded
  4. protein threaded through proteasome
  5. proteolysis
208
Q

What are proteinopathies?

A

Accumulation of misfolded proteins resulting in aggregates,

thereby gaining toxic activity or losing the normal function.

209
Q

What proteins are associated with early onset familial AD?

A

Amyloid Precursor Protein (APP) (gives rise to amyloid B-peptide)
Presenilin -1, -2

210
Q

What proteins are associated with sporadic AD?

A

ApolipoproteinE e4 allele

211
Q

What change in secondary structure of amyloid protein is associated with AD?

A

Change from an alpha helix to a beta sheet.

212
Q

Tauopathies are characterised by what abnormal modification to tau?

A

Hyperphosphorylation.

213
Q

How is α-synuclein abnormally modified in dementia with Lewy bodies?

A

α-synuclein misfolded into β pleated sheet that aggregate to form fibrils.

214
Q

What are Transmissible Spongiform Encephalopathies (TSEs) / Prion diseases?

A

A family of rare, progressive & fatal neurodegenerative disorders associated with loss of motor coordination and behavioural changes.

215
Q

Describe the pathological changes seen in TSEs? What is the aetiological agent of these conditions?

A

Characteristic spongiform changes associated with neuronal loss,
and a failure to induce an inflammatory response.
Prions.

216
Q

Name two examples of TSEs and their routes of transmission.

A

Kuru - ritualistic cannibalism

Variant Creutzfeld-Jakob Disease (CJD)- ingestion of contaminated food.

217
Q

Name a few specific tests that can be used to assess attention.

A

STROOP test - colours and words
Spell WORLD backwards
Serial 7s

218
Q

What is the difference between retrograde and anterograde amnesia?

A

Retrograde - forgetting past events

Anterograde - forgetting new experiences and info

219
Q

What is Ribot’s gradient?

A

Forget more recent material first and then will start to forgot older information as the disease progresses

220
Q

What is the difference between explicit and implicit memory?

A

Explicit - requires conscious thought

Implicit - does not require conscious thought

221
Q

Which part of the brain is responsible for implicit memory?

A

basal ganglia, cerebellum, cortex

222
Q

What is working memory? What part of the brain is responsible for it?

A

Temporary holding and using of information for a short period of time.
Frontal lobe - DLPRC

223
Q

Define episodic and semantic memory? Where in the brain is responsible for these?

A

Episodic - memory of autobiographical events - medial temporal lobe
Semantic - general knowledge, words, meaning of words -

224
Q

Describe the spectrum of cognitive impairment.

A

Age related decline
Mild cognitive impairment (MCI)
Dementia

225
Q

What is the total cost of dementia to society?

A

£26.3 billion

226
Q

What investigations can be used in dementia?

A
  • FBC
  • ESR, CRP
  • Glucose
  • U+E
  • LFTs
  • Bone profile
  • TFTs
  • Urinalysis, MSSU
  • B12, folate
227
Q

What are the different diagnostic components of dementia?

A
  • Clinical assessment
  • Corroborative history
  • General physical examination
  • Mental State Examination
  • Standard (+/- specialised) bloods
  • Structured cognitive testing
  • Structural (+/- functional) imaging
228
Q

What different cogntitive tests can be used for dementia assessment?

A

MMSE
Abbreviated mental test (AMT)
Addenbrooke’s cognitive assessment (ACE III)
6 Item Cognitive Impairment test (6CIT)

229
Q

What are some non-pharmacological approaches to managing delirium?

A
  • Noise control and lighting
  • Orientating influences – calendars, clocks, familiar objects, family (reality orientation)
  • Fluid balance/diet/bowel habit/pain control
  • Regular communication/reassurance from staff. Address sensory impairment
  • Limit variation in staff
  • Encourage normal sleep cycle and side room if possible
  • Early mobilising
  • Avoid ward transfers
  • Consider necessity of certain procedures
  • Recognise frailty
230
Q

What are some pharmacological approaches to managing delirium?

A 
Antipsychotics
•Haloperidol
•Olanzapine
Benzodiazepines
•Lorazepam
•Diazepam
Others
Specific treatment of underlying cause
•Melatonin
231
Q

What are the pharmacological options for treating dementia?

A

Cholinesterase inhibitors i.e. rivastigmine, donepezil - for mild-moderate AD and PDD
Glutamate receptor antagonist i.e. memantine -for moderate to severe AD

232
Q

What are some of the side-effects associated with cholinesterase inhibitors in treating dementia? Include serious adverse effects.

A

Nausea, vomiting, diarrhoea, muscle cramps, dizziness, fatigue, anorexia.
Serious: cardiac adverse effects, peptic ulcers/GI bleeding.

233
Q

Give an outline of different types of cancer treatments available.

A

Non-cellular therapies: cytokine therapy - TNF-alpha/beta, IL-2 therapy. Immunotherapy: Nivolumab, ipilimumab, vemurafenib.
Cellular therapies: Haemapoetic stem cell, tumour infiltrating T cells, dendritic cell vaccines, NK cells, gamma-delta T cells, genetically engineered T cells. Virus specific T cells.

Year 2 Revision (15 decks)

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